This document is a lecture note on obstetrics and gynecology for health science students. It is divided into 5 sections that cover the basics of reproductive anatomy and physiology, normal and abnormal pregnancy, normal and abnormal labor, the normal and abnormal postpartum period, and gynecology. The note is intended to standardize training across institutions and provide a quick reference for students and instructors. It emphasizes the detection, diagnosis, and management of common obstetric and gynecologic emergencies that health officers would encounter.

1. OBSTETRICS AND
GYNECOLOGY
FOR
Health Science Students
Lecture Note
Hawassa Health Sciences College
Hawassa University

2. Obstetrics and Gynecology
For
Health Science Students
Lecture Note
Samson Negussie, Assistant Professor
M.D. Obstetrician and Gynecologist
April 2006
In collaboration with The Carter Canter (EPHTI) and The
Federal Democratic Republic of Ethiopia Ministry of
Education and Ministry of Health

3. TABLE OF CONTENTS
Preface i
Acknowledgement ii
About the lecture note iii
Abbreviations v
SECTION ONE – BASICS
CHAPTER 1 Reproductive anatomy, physiology and embryology 1
CHAPTER 2 Obstetric and gynecology evaluation 9
SECTION TWO – NORMAL AND ABNORMAL PREGNANCY
CHAPTER 3 Normal physiology and diagnosis of pregnancy 17
CHAPTER 4 Common minor disorders of pregnancy 22
CHAPTER 5 Antenatal care 27
CHAPTER 6 Abnormal bleeding during first and second trimesters of
pregnancy
31
CHAPTER 7 Antepartum hemorrhage 44
CHAPTER 8 Hypertensive disorders of pregnancy 49
CHAPTER 9 Disturbances of amniotic fluid 55
CHAPTER 10 Premature rupture of membranes and preterm labour 58
CHAPTER11 Multiple pregnancy 63
CHAPTER12 Rh isoimmunization 67
CHAPTER13 Medical disorders of pregnancy 70
SECTION THREE – NORMAL AND ABNORMAL LABOUR
CHAPTER 14 Physiology and management of normal labour 84
CHAPTER 15 Induction and augmentation of labour 92
CHAPTER 16 Operative deliveries 97
CHAPTER 17 Malpresentations and malpositions 105
CHAPTER 18 Dystocia 115
CHAPTER 19 Obstructed labour and ruptured uterus 121
CHAPTER 20 Fetal distress 127
SECTION FOUR – NORMAL AND ABNORMAL PEUPERIUM
CHAPTER 21 Normal puerperium and its management 131
CHAPTER 22 Postpartum hemorrhage 135
CHAPTER 23 Postpartum complications 141
SECTION FIVE – GYNECOLOGY
CHAPTER 24 Menustral cycle and its abnormalities 147
CHAPTER 25 Climacteric and related problems 158
CHAPTER 26 Vaginal discharge and vulvar pruritis 161
CHAPTER 27 Pelvic inflammatory disease 167
CHAPTER 28 Family planning 171
CHAPTER 29 Infertility 179
CHAPTER 30 Tumor conditions of the female genital tract 183
CHAPTER 31 Uterovaginal prolapse and urinary incontinence 193
PREFACE
Ethiopia is one of the countries in the world with unacceptably high maternal mortality rate.
Various strategies are being implemented to reduce this rate and improve the overall health
of women. One such strategy is ensuring the provision of preventive, curative and
i

4. rehabilitative health services to the population by improving access and quality of services by
training competent midlevel and front line health workers.
Currently a number of higher learning institutions are involved in the training of health
officers. One of the objectives of health officer training is producing competent professionals
capable of delivering comprehensive emergency obstetric care and managing other common
gynecologic problems.
One of the problems encountered during the training is shortage of standardized training
materials gauged to meet the objective of the health officers training. Different training
institutions use different text materials and the emphasis given to different topics varies. The
emphasis given to common obstetric and gynecologic topics prevalent in resource poor
countries varies greatly.
The Ethiopian Public Health Training Initiative (EPHTI) has recognized this critical problem
and was involved in development of standardized training materials (modules and lecture
notes) in different public health and clinical subjects.
This lecture note is prepared to help in standardizing the training in different teaching
institutions. It also aims to provide a quick reference for students and is believed to initiate
further reading. This final version was designed and prepared to address the needs of health
officer training. It emphasizes mainly on detection, diagnosis and management of emergency
obstetrics problems and common gynecologic diseases.
ii

5. ACKNOWLEDGEMENT
My deepest gratitude goes to The Carter Center and the Ethiopian public health training
initiative for providing technical and financial support. Special thanks goes for Ato Aklilu
Mullugeta whose unrelenting follow up made this lecture note a reality. The following people
were involved in the development of the first draft and need to be credited: Dr. Habtemariam
Tekle (Gondar University), Drs. Fassil Mengistu and Endris Mohammed (Debub University),
Dr Mussie Abera (Alemaya University) and Dr. Zerai Kassaye (Jimma University).
I am highly indebted to Dr. Solomon Kumli, Dr. Yirgu G/Hiwot of Addis Ababa University,
Gynecology and Obstetric department for their constructive comments and suggestions
without which this lecture note wouldn’t have takes its present shape.
iii

6. ABOUT THE LECTURE NOTE
Organization
This lecture note is organized into five sections. The first section deals with the basic topics
needed to deal with obstetrics and gynecology. A short summary of anatomy, physiology and
embryology of the female genital tract is followed by an outline of obstetric/ gynecologic
history and physical examination. The second section deals with normal changes of
pregnancy, antenatal care and various antenatal complications of pregnancy. The third
section gives description of normal and complicated (abnormal) labour along with their
management. The fourth section is entitled for puerperium and abnormalities associated with
postpartum period. The final section deals with normal menustral cycle and different
gynecologic problems. Review questions follow each chapter. Because of repetition of
reference materials used for each topic, the author preferred to give references for the
different topics are given at the end of each section. Malpresentations are included in section
three (normal and abnormal labour) because of their importance in terms of maternal and
neonatal complications is related to their occurrence in labour and the need to stress the
different emergency maneuvers used in malpresentation for a health officer student. In
section five (gynecologic section) related topics are lumped under one chapter. Tumor
conditions of the female genital tract are organized into benign and malignant conditions.
Preparation
Preparation of this lecture note was started some 18 months back. Representatives from four
different universities (Alemaya, Jimma, Gondar and Debub now Awassa) divided the topics
among themselves and took the task of developing the first draft. The then Debub University
(now Awassa University) took the task of compiling and editing the first draft. During this
reviewing/ editing process a number of problems were encountered. The major one is most
of the draft developed was so detailed and did not take into consideration the level of
competence required of a health officer. The other is failure to get the first draft from some of
the universities in time. Internal reviewing done on the available draft suggested significant
remodeling to be done on the first draft. Modification/ rewriting of the first draft to meet the
above objective could not be done in time because of the fact that most of the professionals
involved in the development of the first draft left their respective universities. So finalization of
the lecture note was delayed. After discussion with the responsible people in The Carter
Center, the author took the responsibility of reshaping and rewriting the final version of this
lecture note. During this preparation the curriculum for health officer training, the first draft
iv

7. and different references were consulted and appropriate modifications were made. Financial
and other technical support was provided by The Carter Center.
This final version was designed and prepared to address the needs of health officer training.
It emphasizes mainly on detection, diagnosis and management of emergency obstetrics
problems and common gynecologic diseases. Conditions that can not be diagnosed/
managed at a health center setting and/ or require specialist care are omitted or are briefly
mentioned.
Application
This lecture note is designed to be used by a health officer student as a guide for further
reading. It can also be used as a quick reference by other cadre of health science students
(medical students, midwives and nurses) taking obstetrics and gynecology as part of their
training. It can be used as a reference by instructors of Obstetrics and Gynecology.
Limitations
This lecture note is by no means a replacement for standard texts in obstetrics and
gynecology. It only gives an outline of the important aspects of the topics that are relevant for
health officer training. It omits detailed description of some aspects of the topics involved.
Some topics not included in the curriculum are not included in this lecture note. Sophisticated
and recent diagnostic/ treatment modalities not applicable in the setting a health officer works
and details of pathogenesis are not given due emphasis. The user is thus advised to use the
mentioned references for such details.
v

8. ABBREVIATIONS
ACTH – Adrenocorticotrophic hormone
AFI – Amniotic fluid index
ANC – Antenatal care
ARM – Artificial rupture of membranes
APH - Antepartum hemorrhage
AUB – Abnormal uterine bleeding
BPD – Biparietal diameter
CPD – Cephalopelvic disproportion
C/S – Caesarian section
DNA – Deoxyribonucleic acid
DUB – Dysfunctional uterine bleeding
DVT – Deep vein thrombosis
E&C/ D&C – Evacuation and curettage/ dilatation and curettage
EDD – Expected date of delivery
FHB – Fetal heart beat
GH – Growth hormone
GTD – Gestational trophoblastic tumors
HCG – Human chorionic gonadotrophic hormone
HDP – Hypertensive disorders of pregnancy
HPO – Hypothalamo pitutary ovarian axis
IUCD – Intrauterine contraceptive devise
LMP/LNMP – Last menustral period/ last normal menustral period
MSH – Melanocyte stimulating hormone
MTCT – Mother to child transmission
MVA – Manual vacuum aspiration
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9. OCP – Oral contraceptive pills
OL – Obstructed labour
PAC – Post abortion care
PID – Pelvic inflammatory disease
PIF – Prolactin inhibitory factor
PIH – Pregnancy induced hypertension
PMI - Point of maximum impulse
PMS - Premenstrual syndrome
PPH - Post partum hemorrhage
PROM - Premature rupture of membranes
POP – Progestin only pills
RH - Rhesus factor
STD/STI – Sexually transmitted diseases/ sexually transmitted infections
TORCH
TSH – Thyroid stimulating hormone
UTI – Urinary tract infection
VDRL – Venereal disease research laboratory
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10. Obstetrics and Gynecology
PART I: BASICS
CHAPTER 1
REPRODUCTIVE ANATOMY, PHYSIOLOGY
AND EMBRYOLOGY
By Dr. Habtemariam Tekle
Learning objective
To know the anatomy of the female reproductive system
To know the physiology of the female reproductive system
To know the normal development of the female genital tract
Introduction
It is mandatory to know the anatomy and physiology of the female reproductive system to
manage obstetric and gynecologic problems.
1. ANATOMY OF THE FEMALE PELVIC ORGANS
1.1. External female genitalia (vulva or pudendum )
1.1.1. Anatomic landmarks
The vulva includes mons pubis, labia majora, labia minora, clitoris, vestibule and perineum
which are all visible on external examination. It is bounded anteriorly by the mons pubis,
laterally by the labia majora and posteriorly by the perineum.
A. Mons Pubis
It is the pad of subcutaneous fatty tissue in front of the pubis. It is covered by the pubic hair
in inverted triangle fashion.
B. Labia majora
It is the elevation skin and subcutaneous tissue which forms the lateral boundaries of the
vulva. Posteriorly each labia majora fuses medially to form the posterior commissure. The
labia majora contains sebaceous glands, sweat glands and hair follicles. The dense
connective tissue and adipose tissue beneath the skin is richly supplied with venous plexus
which may produce hematoma, if injured. The labia majora are homologous with the scrotum
in the male.
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11. Obstetrics and Gynecology
C. Labia minora
These are two thick skin folds, devoid of fat, lying on either side within the labia majora.
Anteriorly they are divided to enclose the clitoris and unite with each other in front and behind
the clitoris to form the prepuce and frenulum respectively. Posteriorly each labia minora fuse
to form a fold of skin called fourchette. Labia minora don not contain hair follicle. It is
homologous with the ventral aspect of the penis.
D. Clitoris
This is a small cylindrical erectile body situated in the most anterior part of the vulva. It
consists of the glans, body and two crura. It is analogous to the penis in the male.
E. Vestibule
It is a triangular space bounded anteriorly by the clitoris, posteriorly by the fourchette and on
either side by labia minus. There are erectile tissues bilaterally situated beneath the mucus
membrane called the vestibular bulb. Each bulb lies anterior to the Bartholin’s gland and is
incorporated within the bulbocavernous muscles. They are homologous to the single bulb of
the penis and corpus spongiousum in the male.
There are four openings into the vestibule.
I. Urethral opening which is situated in the midline just anterior to the vaginal orifice.
II. Vaginal orifice which is located posterior to the urethral opening. In virgins and
nulliparous the opening is closed by the labia minora but in parous, it may be
exposed. The orifice is incompletely closed by a septum of mucus membrane called
hymen.
III. Bartholin’s duct opening (one on each side): The Bartholin’s glands are situated
in the superficial perineal pouch posterior to the vestibular bulb. It secretes abundant
alkaline mucus, during sexual excitement which helps in lubrication. Each gland has
got a duct which opens just anterior to the Hymen. The Bartholin’s gland
corresponds to the bulbourethral gland in the male.
F. Perineum (Perineal body)
This is a pyramidal shaped tissue where the pelvic floor and the perineal muscles and fascia
meet. It is located between the vagina and the anal canal.
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12. Obstetrics and Gynecology
1.1.2. Blood supply of the Vulva
A. Arteries
Branches from the internal pudendal arteries (labial artery, transverse perineal artery, artery
to the vestibular bulb and deep and dorsal arteries to the clitoris) and femora artery
(superficial and deep pudendal arteries) supply the different parts of the vulva.
B. Veins
The veins of vulva form plexus and drain into internal pudendal vein, vesical or vaginal
venous plexus and the long saphenous vein.
1.1.3. Nerve supply to the vulva
It is supplied by cutaneous branches from the ilioinguinal, genital branches of genitofemoral
nerve, pudendal branches from the posterior cutaneous nerve of the thigh and labial and
perineal branches of pudendal nerve.
1.2. Internal female genital organs
The internal genital organs in female include vagina, uterus, fallopian tubes and the ovaries.
These require special instruments for inspection.
A. Vagina
It is a fibro-musculo-membraneous canal communicating the uterine cavity to the exterior at
the vulva. It has four walls: anterior, posterior and two lateral walls. The length of the anterior
wall measures 7 centimeters and the posterior wall is about 9 centimeters. The projection of
the cervix through the anterior vaginal wall at the top of the vagina (vault) creates clefts
known as fornices. There are four fornices (anterior, posterior and two lateral).
Its wall is composed of four layers. The four layers from within to outwards are mucus
membrane lined by stratified squamous epithelium, sub mucous layer, muscular layer( inner
circular and outer longitudinal) and fibrous coat.
The vaginal secretion is very small but sufficient to make the surface moist. The pH is acidic
and ranges between 4.0- 5.5 in reproductive age groups. The Doderlin’s bacilli are
responsible for conversion of Glycogen from the exfoliated squamous cells to lactic acid.
The vagina serves as excretory channel for menstrual blood and uterine secretions, organ for
sexual intercourse and passage for the fetus during birth.
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13. Obstetrics and Gynecology
Blood supply
The arteries supplying the vagina are cervico vaginal branch of the uterine artery, vaginal
artery (a branch fro internal iliac artery), and middle rectal and internal pudendal artery.
These anastomose with one another and form two azygous arteries, one anterior the other
posterior.
Veins drain into internal iliac and internal pudendal veins.
B. Uterus
This is a hollow pyriform muscular organ situated between bladder and rectum. It is normally
anteverted and anteflexed. It measures 8 centimeters long, 5 centimeters wide and 1.25
centimeters thick. It has three parts.
I. Body or corpus which is the part between the isthmus and the opening of the
fallopian tubes. The part that is above the opening of the fallopian tubes is called
the fundus.
II. Isthmus is a constricted part situated between the body and the cervix. It measures
about 0.5 centimeters.
III.Cervix is the lower most part of the uterus which is cylindrical in shape and
measures about 2.5 centimeters. It is divided into supravaginal part (part lying
above the vagina) and portiovaginalis (which lies within the vagina). It has two
openings the internal os and the external os with cervical canal in between.
The uterine wall consists of three layers.
I. Perimetrium is the serous coat covering the underlying myometrium
II. Myometrium consists of thick bundles of smooth muscles arranged in various
directions.
III. Endometrium is the mucus lining of the endometrial cavity. It consists of the
surface epithelium and laminia propiria.The surface epithelium is a single layer of
ciliated columnar epithelium and the lamina propria contains stromal cells,
endometrial glands, vessels and nerves.
Blood supply
The arterial supply is mainly from the uterine artery and the other sources are vaginal and
ovarian arteries.
The venous channel corresponds to the arterial course and drain into internal iliac veins.
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14. Obstetrics and Gynecology
C. Fallopian Tube
The uterine tubes are paired structures which are attached to the lateral angle of uterine
cavity. It has four parts intramural or interstitial (part inside the uterine wall), the isthmus (the
straight part), ampulla (the tortuous part) and the infundibulum. The abdominal ostium is
surrounded by a number of radiating fimbria, one of these is longer than the rest and is
attached to the outer pole of the ovary - ovarian fimbria.
D. Ovary
Ovaries are paired sex glands or organs. Each measures 3centimetres by 2 centimeters by 1
centimeter. Each is attached to the uterus by the utero-ovarian ligament, to the lateral pelvic
wall by infundibulopelvic ligament and to the posterior wall of the broad ligament by the
meso-ovarium.
They are covered by a single layer of germinal epithelium. The substance of the ovary has
cortex and medulla. The cortex is the functional layers which include primordial follicles,
mature follicles, Graffian follicles, corpus luteum and atretic follicles or corpus albicans.
Medulla consists of loose connective tissue, muscle cells, blood vessels and nerves and
hilus cells.
Blood supply
Arterial supply is from the ovarian artery, a branch of the abdominal aorta. Venous drainage
is through pampiniform plexus to form ovarian veins which drain to inferior vena cava on the
right side and to the left renal vein on the left side.
Nerve supply
It receives sympathetic supply from T10.
2. PHYSIOLOGY OF THE FEMALE REPRODUCTIVE ORGANS
The physiology of female reproductive system is concerned with the functions from birth
through puberty and adult hood to the menopause. This is achieved through the
neuroendocrine mechanism that involves the cortico-hypothalamic-pituitary-ovarian axis. The
hypothalamo pitutary ovarian axis is a well coordinated axis and the hormones liberated from
the hypothalamus, pituitary and the ovary are dependent on one another.
The secretion of the hormones from these glands is modified through feedback mechanisms
operating through this axis. The axis may also be modified by hormones liberated from the
thyroid and adrenal glands.
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15. Obstetrics and Gynecology
A. Hypothalamus
It produces specific releasing and inhibitory hormones or factors which have effect on the
production of pituitary hormones.
I. Gonadotrophic releasing hormones (GnRh) is concerned with the synthesis storage
and release of gonadotrophic hormones, FSH and LH.
II. Prolactin inhibitory factor/ hormone (PIF) inhibits the release of prolactin.
III. Thyrotrophin releasing hormone (TRH) stimulates the release of TSH.
IV.Corticotrophin releasing hormone (CRH) stimulates the release of ACTH.
V. Growth hormone releasing hormone stimulates the release of growth hormone.
B. Pituitary
It has two parts, the anterior pituitary (adenohypophysis) and the posterior pituitary
(neurohypophysis).
The adenohypophysis produces
I. Gonadotrophins which include follicle stimulating hormone (FSH) and leutinizing
hormone (LH). FSH is mainly stimulates the growth and maturation primary ooytes of
which only one develops into graffian follicle. In conjunction with LH, it is also involved
in ovulation and steriodeogenesis. The main function of LH is steriodeogenesis but
along with FSH, it is responsible for full maturation of the Graffian follicle and
ovulation.
II. Prolactin is responsible for the production of the milk in the breast.
III. The other hormones TSH (thyroid stimulating hormone), ACTH (adrenocorticosteroid
hormone), GH (growth hormone) and MSH (melanocyte stimulating hormone).
C. Ovary
The function of ovary is ovulation and production of ovarian hormone. The major ovarian
hormones are estrogen and progesterone, also called the female sex hormones. The other
hormones produced by the ovary are androgens and inhibin.
Estrogen is produced by granulosa cells. Its functions include
I. Development of female secondary sexual characteristics including deposition of fat in
the breast, thighs & hips and growth and development internal & external female
genital organs.
II. Decreases FSH and LH secretion by negative feedback mechanism during the
menstrual cycle except at mid cycle at which time it increases LH secretion by
positive feedback mechanism.
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16. Obstetrics and Gynecology
III. In the breast it stimulates the growth of the ducts and fat deposition.
Progesterone is secreted by the lutenized theca granulosa cells. Its functions are
I. Increases the glandular secretions of the endometrium and diminishes the
contractility of myometrium.
II. Stimulates the growth of the acini in the breast.
III. In large doses it inhibits LH secretions.
IV. Increases basal body temperature.
Androgens are produced mainly by the theca interna cells. They are source for estrogen
synthesis. Inhibin and relaxin are other hormones produced by ovary.
Hypothalamo-Pituitary-Ovarian (HPO) Axis at different stages of life
I. Fetal life- HPO axis remains active and functional from 20 weeks of life.
II. Infancy and childhood- high level of FSH and LH at birth gradually decline and
minimum level achieved by two years of age.
III. Prepuberity – hypothalamus is very much sensitive to negative feedback by even a
small amount of estrogens (estrogen produced by peripheral conversion of
testosterone to estrogen). Hence, FSH and LH secretions are inhibited.
IV. Puberty –hypothalamus become more insensitive to estrogen to estrogen negative
feedback. Hence increasing amounts of GnRH, FSH and LH are secreted, which in
turn stimulate the ovary to secrete estrogen and progesterone. This eventually results
in thelarche, adrenarche and menarche.
V. Pregnancy- the gonadotrophins level remains low.
VI. Menopause- ovarian follicles become scarce and resistant. Hence FSH and LH
levels increase while estrogen and progesterone levels decrease.
3. EMBRYOLOGY OF THE REPRODUCTIVE ORGANS
Introduction
In early pregnancy, both internal and external genital organs are undifferentiated. During
development, because of “X” and “Y” chromosomes and other hormones, the
undifferentiated genitalia differentiate either to male or female genital organ. Male sex is an
induced sex because it requires specific messages to develop. Genital and urinary systems
are in close proximity. During development of one system induces the development of the
other system. This explains why congenital malformations of genital system are often
associated with abnormalities of urinary and musculoskeletal system.
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17. Obstetrics and Gynecology
Development of gonads
On fourth week after fertilization, primordial germ cells migrate from yolk sac through the
mesentery of the hind gut to the posterior body wall mesenchyme at the tenth thoracic level.
Their arrival induces proliferation of adjacent mesonephros and celomic epithelium to from
the genital ridge. The celomic epithelium forms the cortex, the mesenchyme forms the
medulla and the germ cells originate from the endoderm. This stage of gonadal development
is called the indifferent stage (bipotential gonads).
Further development is influenced by the Y chromosome which has the sex determining
region (SRY). In its presence the indifferent gonad develops into testis. In its absence like in
XX or XO fetus it develops into an ovary.
In further development of the ovary the medulla regresses to form rete ovary and the cortex
forms the ovarian follicles. Between the seventh and ninth months the ovary descends to the
pelvis to be attached to the ligaments.
Development of internal female genital organs
Two major ducts give rise to the internal genital organs, namely the Wollfian duct (male duct)
and the Mullerian duct (female duct). In the presence of testis the Wollfian duct develops
(effect of testosterone produced by Leydig cells) and the Mullerian duct regresses (effect of
Mullerian regressing factor produced by the Sartoli cells). But, in the absence of functional
testis the reverse happens. The Mullerian duct is formed by invagination of celomic
epithelium. The two Mullerian ducts grow downwards and medially. Eventually their lower
ends fuse into one. Further development results in cavitations to form hollow organs at fifth
month of gestation.
The fallopian tubes develop from upper unfused horizontal part of the Mullerian duct. Uterus
develops from intermediate horizontal and adjoining vertical part of Mullerian duct. The lining
epithelium and glands develop from coelomic epithelium. Myometrium and endometrial
stroma arise from mesoderm. Broad ligament is formed as a broad transverse fold as the
Mullerian ducts approach midline. It extends from lateral side of fused duct to pelvic side
wall. It has vestigial remnants like epoophoron, paroophoron and ducts.
Vagina is formed in third month of gestation. There are two concepts for the development of
vagina. One says the whole vagina is developed from the urogenital sinus. The other argues
that vagina is mainly developed from Mullerian duct with only one third contributed by the
urogenital sinus.
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18. Obstetrics and Gynecology
Development of External genital Organs
In the fifth week of embryonic life, folds of tissue form on each side of cloacae. Development
of coronal partition, called urorectal septum, separates the endodermal cloacae into two
parts. The dorsal part, which at its lower end is covered by the anal membrane, develops into
rectum and anal canal. The ventral part which is now called the urogenital sinus develops
into the external genital organs. It lower end is lined by the bilaminar urogenital membrane.
The site of fusion between urorectal septum and the urogenital membrane is the primitive
perineal body.
Further development of the urogenital sinus differentiates it into three parts. The upper or
vesicourethral part forms the mucus membrane of bladder and major part of female urethra.
The middle pelvic part receives the united caudal part the two paramesonephric (Mullerian)
ducts in the midline. It later gives rise to the epithelium of the vagina, the Bartholin’s gland
and the hymen. The lower phallic part is lined by the bilaminar urogenital membrane. The
phallic part has one genital tubercle, and two genital folds and urogenital swellings
(labioscrotal folds).
Clitoris is developed from the genital tubercle. Labia minora are developed from the genital
folds. Labia majora are developed from urogenital swellings (labioscrotal swellings).
Bartholin’s Glands develop as out growth from the caudal part of the urogenital sinus.
Vestibule develops as urogenital groove from urogenital sinus. Hymen is developed from the
junction of the sinovaginal bulbs and urogenital sinus.
Some congenital malformations
Failure of development of both mullerian ducts results in absence fallopian tubes, uterus, and
upper two thirds of vagina (Mullerian agenesis).
Failure of development of one mullerian duct results in unicornuate uterus with single
oviduct.
Failure of recanalization of the lower part of the fused Mullarian duct results in isolated
atresia of upper vagina and cervix causing hematometra.
Failure of fusion of mullerian duct depending on the degree results in uterus didelphys with
two cervix and vagina canals, arcuate uterus and uterus bicornis.
Fallopian tube abnormalities are not common. Rarely accessory ostia or diverticulum or
abnormally short or long tubes may occur.
Failure of canalization of the urogenital membrane results in imperforate hymen. Failure of
development of the external genitalia results in ambiguous genitalia.
Reminants of Wollfian duct result in Gartner’s cyst found in the upper part of the vagina.
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19. Obstetrics and Gynecology
CHAPTER 2
OBSTETRIC AND GYNECOLOGIC EVALUATION
By Dr. Habtemariam Tekle
Learning objective:
· To enable the student take proper history and physical examination to reach to the
diagnosis.
Introduction
To come to a clear understanding of a patient’s problem, detailed history and physical
examination is important.
1. OBSTETRICS HISTORY & PHYSICAL EXAMINATION
1. History
1.1. Identification
· Name
· Age – significant if less than 20 years and greater than 35 years
· Martial status
· Address- far distance from health institution
· Religion
· Occupation
· Date of admission
· Ward and bed number
1.2. Chief complaints-
Patients may have come for routine antenatal care follow up or may come with one or more
specific complaints. Note the duration of each complaint.
1.3. History of present pregnancy
Get information on the following points
· Gravidity- all forms of pregnancy whether it is term, live births, still birth, abortion,
ectopic pregnancy or molar pregnancy.
· Parity- fetus delivered after 28 weeks of gestation for Ethiopia and United kingdom
and greater than or equal to 20 weeks – according to WHO
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20. Obstetrics and Gynecology
· Abortion
· Last normal menstrual period (LNMP)
· Expected date of delivery (EDD) which could be calculated by
1- Naegale’s rule (using European calendar)
- LNMP- 3 months + 7 days
2- Ethiopian calendars
· NLMP+ 9 months +10 days if pagume is not passed
· NLMP+ 9 months + 5 if pagume is passed ( 4 in leap year )
· Calculate gestational age in completed weeks and days
· Quickening – the first time the mother felt fetal movement
- In primigravida it is around 18-20 weeks and in multigravida
at 16-18 weeks of gestational age.
- Used to date pregnancy if LNMP is unknown
· Presence of antenatal care elsewhere. place and number of visits.
· Elaboration of chief complaints
· Danger symptoms of pregnancy (vaginal bleeding, severe headache, blurring
of vision, epigastric or severe abdominal pain, profuse vaginal discharge,
absence or reduction of fetal movement, fever, persistent vomiting)
· Common complaints in pregnancy ( like nausea and vomiting, weakness
· Pregnancy - unplanned , unwanted and unsupported
· Ask positive and negative statement according to the patient complaints
1.4. Past obstetric history
The following should be asked for all previous pregnancies in chronologic order
· Date, month and year of gestation for example first delivery in May 2000
· Length of gestation - abortion (< 28 weeks), preterm (<37 completed
weeks), term (>37 completed to 42 completed weeks), post term (greater
than 42 completed weeks)
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21. Obstetrics and Gynecology
· Significant antenatal medical problems like hypertension, ante partum
hemorrhage, diabetes
· Onset of labor (spontaneous or induced)
· Fetal presentation
· Duration of labor
· Mode of delivery (spontaneous vaginal, instrumental, caesarian section,
destructive delivery)
· Fetal outcome (alive or dead, sex of the newborn, weight of the newborn,
malformations, current condition)
· Post partum complications postpartum hemorrhage
1.5. Gynecology history
· Family planning methods - use , type , duration and side effects
· Sexual history- assess risk of sexually transmitted infections and
HIV/AIDS
· Gynecology operations- Female genital mutilation , laparatomy, dilatation
and curettage ,evacuation and curettage, manual vacuum aspiration
· Menstrual history ( age of menarche, interval of period 21-36 days,
amount of flow 10 –80 ml, duration of flow 1-8 days, normally dark red and
non-clotting).
1.6. Past medical and Surgical History
· History of diabetes mellitus, hypertension, hypo or hyper thyroidism
which may the affect pregnancy or get aggravated by pregnancy
· Blood transfusion important in hemolytic disease of new born
· Drugs risk of teratogenicity or allergic reactions
· Maternal infection – TORCH Syndrome.
1.7. Personal, family and social history
· Childhood development
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22. Obstetrics and Gynecology
· Educational status
· Habits like alcohol , smoking and elicit drugs
· Occupation- exposure to radiation, anesthesia- halothane, chemical
factory and others
· Income- low socio-economic status associated with obstetric problems like
preeclampsia ,preterm labor
· Family history- diabetes mellitus, hypertension, multiple pregnancy,
genetic disorders
1.8. Review of Systems
· Check all systems
2. Physical examination
Examination must be done in a private room in the presence of a chaperone. Proper
explanation must be offered to the patient before during and after the examination. Bladder
should be emptied and the patient properly positioned on the couch. Warm hands and
instruments must be used. Adequate light, appropriate gloves and swabs should be
prepared. Always keep eye contact throughout the examination.
2.1. General appearance
2.2. Vital signs and anthropometric measurements
· Blood pressure positions include left lateral with 300 tilt to the left to avoid
supine hypotensive syndrome or sitting position in ambulatory patient.
· Pulse rate -increases 10-15 beats/minute in pregnancy
· Respiratory rate -increases 1-4 breath /minute in pregnancy
· Temperature
· Weight – increment of more than 1kg/week is abnormal
· Height- less than 150 centimeters could be constitutional but may be a
risk factor. Strikingly short for every society is risk factor.
2.3. HEENT
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23. Obstetrics and Gynecology
· Emphasis on conjunctiva, sclera, teeth and buccal mucus membrane to
see pallor, jaundice, mucosal congestion and dental carries.
2.4. Lymphoglandular System
· Thyroid gland for hyper or hypo thyroidism signs.
· Breast for nipple refraction, pigmentation, lumps, discharge, colour change
2.5. Respiratory and cardiovascular system
Steps in examination are essentially same as non pregnant patient. Note that
the following are normal findings in pregnancy.
· Decreased diaphragmatic excursion due to diaphragm elevation by gravid
uterus
· PMI deviation to left is possible in pregnancy
· S3 gallop may be heard
· Functional systolic murmur may be heard
2.6. Abdomen
2.6.1Inspection
· Linea nigra- midline hyper pigmentation due to melanocyte stimulating
hormone
· Striae gravidarum – purplish in new striae and white in old striae. In both
cases is due to distension, which causes stretching.
· Umbilicus may be inverted, flat or everted
· Surgical or non surgical scar
· Distended veins, flank fullness, fetal movement
2.6.2. Palpation
· Superficial palpation – checks for rigidity, tenderness, superficial mass and
characterize it, abdominal wall defects.
· Deep palpation – palpate for mass, organomegally and characterize the
mass
· Obstetric palpation or Leopold’s maneuver
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24. Obstetrics and Gynecology
A. The first Leopold maneuver or fundal palpation
I. Fundal height measurement: first correct for asymmetry before
measurement. Then use one of the following methods:
1- Finger method – one finger above umbilicus is equal to two
weeks and below umbilicus one finger is equal to one week.
Uterus felt at symphysis corresponds to 12 weeks. At the
umbilicus it is 20 weeks and at xiphysternum it is 38 weeks.
2- Tape measurement: symphysis to funded height in centimeter
with tape meter between 18-34 weeks is accurate to within two
weeks of actual gestational age.
II. Determine what occupies the fundus. If soft, irregular bulky mass
is found it is the breech. If hard round ballotable mass is found, it is
the head.
B. The second Leopold maneuver or lateral palpation
I. Determines the lie of the fetus which could be longitudinal,
transverse or oblique lie. .
II. In longitudinal lie it determines on which side of the abdomen is the
fetal back. The back of the fetus is linear, rigid and smooth in outline.
The extremities are felt as small irregular and bulky masses. The fetal
heart beat is best heard on back side.
C. The third Leopold maneuver or Pelvic palpation
I. Determines what part of the fetus occupies the lower uterine pole
which is also called the presentation. The possibilities are the head
(cephalic presentation), the breech (breech presentation), and the
shoulder (shoulder presentation).
II. In cephalic presentations it determines the descent by using rule of
fifth which measures the distance between upper border of the
symphysis to anterior shoulder.
5/5 is floating head, 4/5 is fixed head, 2/5 denotes engaged head.
III. In conjunction of the findings of the second maneuver it
determines the attitude of the fetus (relation of head to the trunk). In
extended attitude the cephalic prominence is on the same side of the
15

25. Obstetrics and Gynecology
back. In flexed attitude the cephalic prominence is on the opposite
side of the back. In military attitude the cephalic prominence is felt on
both sides at the same level.
D. The fourth Leopold maneuver or Pawlik grip
It is the only maneuver that is done with one hand. It assesses
presentation of he fetus.
2.6.3. Percussion
· Shifting and flank dullness
· Fluid thrill
2.6.4. Auscultation
· Fetal heart beat is first heard in the back side at16-18 weeks in multiparas
and 18-20 weeks in primigravida. In complete breech it is heard above
umbilicus. In cephalic presentations it is below umbilicus .IN occipito
posterior it is heard in the flanks. .
2.7. Genitourinary system
· Costovertebral and suprapubic tenderness
· Pelvic examination- to be done two times in pregnancy except in cases of
complications and if labor is suspected
I. First trimester (early) – To diagnose pregnancy, for dating of the
pregnancy by measuring uterine size and to diagnose pelvic problems
II. Late in pregnancy greater than 37 weeks
A. To diagnose contracted pelvis (refer chapter on)
- B. To assess Bishop score- (refer to chapter on induction)
III. In labor assess cervical dilatation and effacement, status of the
membranes and color of liquor, presenting part, station of presenting
part and position, molding, caput, clinical pelvimetry.
2.8. Intgumentary system
· Hyper pigmentation on breast, lower and mid line abdomen genitalia are
normally seen in pregnancy
· Vascular Changes- Spider angiomata and palmar erythema
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26. Obstetrics and Gynecology
2.9. Extremities
· Check for edema, dilated vessels and calf tenderness.
Dependent edema (pretibial and pedal), seen in 80% of normal pregnancies.
Pathological edema (non dependent) involves the face, fingers or the whole
body.
2.10. Central nervous system
· As non pregnant
2. GYNECOLOGY HISTORY AND PHYSICAL EXAMINATION
1. History
1.1. Identification
· As obstetric history
1.2. Chief complaints
Patient comes with the following gynecologic complaints. The
common complaints are cessation of menses, vaginal bleeding and
discharge, lower abdominal pain or deep pelvic pain, pain during intercourse
(dysparunia), pain during menstruation (dysmenorrhea), protruding mass
out of the introitus, genital ulcer, urinary incontinence and others.
1.3. History of present illness
· Gravidity, parity and abortion
· Detail of each complaint (localization, duration, date and time of onset,
aggravating and relieving factors, sequence of symptoms, evolution with
time, effect on life style, relation to menstrual cycle and others)
· LMP should be included details of menstrual history if pertinent to the
complaints
· Negative and positive statements pertinent to the presenting complaint
· Treatment received
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27. Obstetrics and Gynecology
1.4. Menstrual history
· Age of menarche
· Interval between period
· Duration of flow
· Amount & character of flow
· Dysmenorrhea , premenstrual symptoms
· Age of menopause
1.5. Gynecologic history
· As obstetric history
1.6. Past obstetric history
· As obstetric history
1.7. Past medical and surgical history
· As obstetric history
1.8. Personal social family, history
· As obstetric history
1.9. Review of systems
· As obstetrics history
2. Physical examination
Preparation for examination is similar to obstetric examination. In addition slides,
applicator, test tube, gloves, speculum and fixative are needed.
2.1. General Condition
2.2. Vital signs
· Blood pressure,pulse rate, respiratory rate, temperature
2.3. HEENT
· As nonpregnant
2.4. Lymphoglandular system
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28. Obstetrics and Gynecology
· Lymph nodes- to see for metastatic cancer check mainly
supraclavicular and axillary nodes.
· Thyroid gland- hypo and hyper thyroidism affects reproductive
function
· Breast examination- inspection and palpation
2.5. Chest and cardiovascular system
· As non pregnant
2.6. Abdomen
· As non pregnant (Inspection, auscultation, palpation and percussion)
2.7. Genitourinary system
· Costovertebral and suprapubic tenderness
· Pelvic examination
I. Examination of external genitalia
Pubic hair- diamond shaped in male and inverted
triangle in female.
Labia majora and minora – ulcer, swelling and
` discoloration
Discharge from urethra and vaginal introitus
Hymen- intact or torn
II.Speculum Examination
Vagina- note color (normally pink), vaginal
septum, rugae folds, fornices, discharge, scar,
laceration
Cervix – note color (normally pink) pink, cervical
os (pin- pointed in nulliparous and slit-like in
multiparous), dilatation, effacement and
bleeding, mass
III. Digital vaginal & bimanual pelvic examination
Vagina- mass and tenderness
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29. Obstetrics and Gynecology
Cervix- Closed normally, moves 2- 4cm with out discomfort,
smooth surface and like tip of nose in
consistency.
Uterus- normally non-tender, mobile, 9 cm in length,
pear shaped smooth and firm.
Adnexa (tubes, ovaries, parametrium and broad ligaments):
normally adenexal structure not palpable except in thin women
with soft abdomen, description of masses.
IV- Rectal and recto vaginal examination
Rectal examination- In virgin and children
Rectovaginal examination- For rectovaginal and uterosacral
ligament nodularity or malignant infiltration
To differentiate rectocele from enterocele
2.8. Intgumentary
· As non pregnant
2.9. Extremities and central nervous system
· As non pregnant
PART II
NORMAL AND COMPLICATED
PREGNANCY
20

30. Obstetrics and Gynecology
CHAPTER 3
NORMAL PHYSIOLOGY & DIAGNOSIS OF PREGNANCY
Learning Objective:
To describe the important physiologic changes in each organ system during pregnancy
To describe the diagnosis of pregnancy
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31. Obstetrics and Gynecology
Introduction-
Pregnancy results in tremendous changes in the physiologic functions of organs, systems
and the body as whole. These changes ensure that the needs of the growing fetus are met
and prepare the mother for parturition and lactation. Changes in the maternal endocrine
system along with hormones produced by the placental / fetal unit are responsible for
majority of the changes. Knowledge about changes due to normal pregnancy is important to
reassure the pregnant woman and manage the minor disorders of pregnancy. Understanding
the normal physiologic changes also gives us the basis to understand the abnormal
conditions during pregnancy.
Terminologies
Pregnancy is a maternal condition of having a developing fetus in the body. It starts at
fertilization where fusion of the ovum (23x) and matured spermatozoa (23x or 23y) takes
place in the fallopian tubes. Zygote (46xx or 46xy) is a cell that results from fertilization. The
zygote divides and redivides forming daughter cells named blastomeres. When the zygote
reaches 16 cell stage, it is named morula. When fluid filled cavity appears in the morula a
blastocyst is formed. The cells of a blastocyst are arranged into layers. The outer layer is
called the trophoblast which eventually develops into the placenta. The inner layer is called
the embryoblast which later gives rise to the fetus. The embryo is the stage after the inner
layer formed two layers (bilaminar disc). The embryonic period is a period where major
structures are formed and extends up to the end of seven weeks after fertilization.
Developing conceptus after the embryonic period is called the fetus. All tissue products of
conception (embryo/ fetus, fetal membranes and placenta) are called conceptus. On day 4
after fertilization the blastocyst enters into the uterine cavity. By day 7, it starts embedding
itself into the prepared endometrium which is now called the decidua. This process is called
implantation.
Placenta and its hormones
The placenta is formed from the trophoblast and decidua basalis. It contains villi covered by
the cytotrophoblast and syncitiotrophoblast. The placental barrier (formed by the
syncitiotrophoblast, cytotrophoblast, the basement membrane and the fetal vascular
endothelial cells) ensures almost complete separation of the maternal and fetal blood. For
this reason the human placenta is of hemo-chorio- endothelial type. In a mature placenta the
villi are grouped into 15- 20 cotyledons, each supplied by one to two spiral arterioles. At 20
22

32. Obstetrics and Gynecology
weeks the discoid placenta reaches full development. The placenta on average has a
diameter of 18 centimeters, a thickness of 23 millimeters, a volume of 497 milliliters, a weight
of 508 grams and villous surface area of
15 square meters. Placenta is a blue red discoid organ with two surfaces. The maternal
surface is made of the decidua basalis with visible septated cotyledons. The fetal surface is
smooth and shiny and is covered by the amnion. The branching fetal vessels are visible
under the amnion.
The placenta acts to the fetus as the lung (exchange of oxygen and carbon diaoxide), gastro
intestinal tract (provision of nutrients), kidney (excretion of hydrogen ion and urea), liver
(detoxifies drugs), immunologic system (transfer of antibodies) and endocrine gland
(production of hormones).
It is connected to the fetus by the umbilical cord or the funis. It has an average length of 50-
60 centimeters (range 30- 100) and diameter of 0.8- 2 centimeters. It contains two umbilical
arteries and one umbilical vein. In addition to acting as conduit for umbilical vessels, it also
allows fetal mobility.
Placenta is a source of incredible amounts of protein and steroid hormones. The major
protein hormone is human chorionic gonadotrophic hormone (HCG), also called the
pregnancy hormone. It has two subunits the alpha and the beta subunits and is produced in
increasing amount to reach a peak between 8 -10 weeks. It maintains the function of the
corpus luteum until the placenta takes over progesterone production. It also plays important
role in male sex differentiation by stimulating testosterone production by the fetal testis. It
also forms the basis for laboratory diagnosis of pregnancy.
In addition placenta produces a number of protein hormones. It is also a source of significant
amounts of progesterone and estrogens. Since placenta lacks some of the enzymes
necessary to synthesize estrogens, it relies on provision os substrates by the fetus and the
mother (fetal-placental –maternal unit).
Organ system changes
I. Cardiovascular system
Cardiac out put increases by 30-50%. The increase in cardiac output is mainly distributed to
the uterus (major share), kidneys, breast and the skin. Heart rate increases by 15-20 % and
stroke volume increases by 25-38%.
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33. Obstetrics and Gynecology
Blood pressure remains largely unchanged with small drop in diastolic pressure. This is the
result of progesterone mediated reduction in peripheral resistance. Blood pressure highest
when seated, lower when supine and lowest when ling on the side. Near term there is a
tendency to develop hypotension when women lie on their back, a condition called supine
hypotension syndrome.
Total blood volume increases up to 45%. Plasma volume increases 35-50% where as red
blood cell volume increases by 20-25%. This results in hemodilution leading to a drop of
hemtocrite and is called physiologic anemia of pregnancy.
Venous pressure rises in lower extremities and central venous pressure unchanged as the
result of pressure by the gravid uterus. This may result in leg edema and development of
varicose veins.
The point of maximum impulse is shifted to the left as the result of elevation of the
diaphragm. Splitting of the first and second heart sounds could be found. High cardiac out
put state may result in gallop and systolic functional murmurs.
II. Respiratory System
Vasodilatations of the nasal vessels result in nasal stuffiness and epistaxis. Diameter and
circumference of chest increase. Altered sense of smell is commonly reported. To meet the
increased oxygen consumption respiratory rate increases. Because of elevation of the
diaphragm by the gravid uterus, diaphragmatic excuration decreases.
III. Alimentary tract
Appetite increases but nausea and vomiting in the morning, which typically occur in the first
trimester, may reduce food intake. Pica (craving for unusual food items of very low nutritional
value like clay and soap) if excessive may result in nutritional deficiencies.
Ptyalism (inability of nauseated women to swallow normal amount of saliva) is an early
symptom of pregnancy. There is no increased production of saliva by the salivary glands.
Gums are edematous and soft. Gum bleeding and acceleration of dental caries from
reduction in oral PH occur. Epulis gravidarum, a tumorous gingivitis with pedunculated
lesions rarely occurs and may cause significant bleeding.
Heartburn due to relaxed esophageal sphincter is a common complaint. Decreased gastric
acid secretion and increased gastric mucus secretion result in relief of symptoms of peptic
24

34. Obstetrics and Gynecology
ulcer disease in majority of women. Delay in gastric emptying is responsible for increased
tendency of aspiration pnumonitis in pregnant women undergoing general anesthesia.
Progesterone induced reduction in peristalsis helps in absorption of nutrients and water from
the small and large intestines. As the result constipation is common and hemorrhoids could
occur.
IN the gall bladder residual volume increases and stasis of bile occurs. This, along with
increased biliary cholesterol saturation, favors gall stone formation.
There are no significant changes in the anatomy of the liver. Liver function tests are normal
except elevation of alkaline phosphatase, whose origin is the placenta. Spider angiomata
and palmar erythema, which are signs of chronic liver disease, are normal findings in
pregnancy.
IV. Urinary System
There is enlargement of the kidneys. The renal calyces and ureters show dilatation which
causes stasis of urine. Bladder tone is also reduced resulting in increased capacity and
incomplete emptying after urination. These changes make a pregnant woman vulnerable to
urinary tract infections.
Renal plasma flow increases by 75% and glomerular filtration rate by 50%. Creatinine
clearance is also increased. Blood urea nitrogen, creatinine and uric acid levels decrease.
Plasma osmolality falls. There is increased glucose and amino acid excretion. Protein loss
amounts to 100-300mg/day.
V. Intgumentary and skeletal system
Vascular changes include spider angiomata and palmar erythema. Cortisol induced changes
in connective tissue result in striae gravidarum. Increased levels of melanocyte stimulating
hormone cause hyper pigmentation of the nipples, areola, axilla, perineum, umbilicus and
linea Alba (forms linea nigra). The mask of pregnancy (chloasma or melasma) is seen on the
cheek bones. Increased secretion of sweat and sebum are other features. Occasionally
pigmented nevi are seen.
In an attempt to maintain the center of gravity, there is exaggerated lordosis and drooping
back of the shoulders. This leads to common complaint of back ache. Parasthesia of the
hands may be caused if there is excessive drooping of the shoulders, which stretch the
brachial plexus.
Loosening of ligaments of symphysis pubis and sacroiliac joint by relaxin causes is aimed to
facilitate vaginal delivery. Pelvic discomfort and gait problems may arise occasionally.
25

35. Obstetrics and Gynecology
VI. Hematology
Red blood cell indices increase. White blood cell counts rise. Platelet count falls. Most
coagulation factors increase creating a hypercoagulable state.
VI. Endocrine & metabolic Changes.
There is massive increase in placental hormones mainly estrogen, progesterone, human
chorionic gonadotrophic hormone and human placental lactogen.
Of the pitutary hormones, follicle stimulating, leutinizing and growth hormones are reduced,
while prolactin levels are high. There is no change in thyroid stimulating and
adrenocorticotrophic hormones.
Thyroid gland shows diffuse enlargement with euthyroid state. There is significant elevation
of plasma cortisol levels.
Pregnancy has a diabetogenic effect due to peripheral insulin resistance caused by high
levels of anti insulin hormones like human placental lactogen.
VII. Genital Systems
Uterus increases in weight from 70 gm of non pregnant state to 1000gm at term. Uterine
blood flow reaches 600ml/minute with 85% supplying the placenta.
Increased vascularity gives the vagina and the cervix bluish color. The cervix becomes soft
from congestion. Increased vaginal discharge may be noted.
Corpus luteum begins to regress at the eight week due to negative feed back mechanism of
estrogen and progesterone on pitutary.
VII. Breast
Both acinar and ductal breast growth occur due to increased estrogen, progesterone and
prolactin levels. Erectile capacity increases. But lactation is inhibited by placental
progesterone which prevents the action of prolactin on the production of lactaalbumin.
VIII. Immune system
HCG reduces immune response of the mother. Serum IgG, IGm and IgA decrease from
tenth week to thirtieth week then they will remain at same level.
IX. Weight gain in pregnancy
On average 12.5 kilograms is gained during pregnancy (range 9kg -15kg).The average
distribution is as follow: the fetus 3300 gm, the placenta 600 gm, amniotic fluid 800 ml, uterus
26

36. Obstetrics and Gynecology
900-1000 gm, breast 400 gm, blood 1200 ml, deposition of fat 2500gm and extra cellular fluid
2600 ml.
Diagnosis of pregnancy
It is based on symptoms, signs and additional investigations.
I. Presumptive findings of pregnancy
· Weakness or fatigue
· Nausea and/or vomiting
· Breast swelling and tenderness
· Increased frequency of Urination
· Amenorrhea
· Discoloration of vaginal mucosa
· Increased skin pigmentation & striae
· Quickening
· Constipation, weight gain
II. Probable findings of pregnancy
· Uterine enlargement
· Change in consistency of cervix & uterus
· Ballottement rebound-16-20 weeks
27

37. Obstetrics and Gynecology
· Braxton Hicks contraction
· Positive pregnancy test
· Symptoms as presumptive finding
III. Positive findings of pregnancy
· Fetal movement perceived by the health personnel
· Fetal heart beat heard by fetoscope (18 weeks) or Doppler (10 weeks)
· Fetal heart beat and fetal body seen by ultrasound
Pregnancy tests
All employ changes in the levels of HCG molecule which can be detected in the maternal
serum as early as nine days. Tests include biologic tests and immunologic tests
(agglutination, radioimmunoassay, radio receptor assay and ELISA).
Review questions
1. Describe the physiologic changes in the cardiovascular system during pregnancy.
2. Discuss the diagnosis of pregnancy.
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38. Obstetrics and Gynecology
CHAPTER 4
MINOR DISORDERS OF PREGNANCY
Learning Objectives
· To describe the minor disorders of pregnancy of pregnancy.
· To discuss the management of the common minor disorders of pregnancy.
Introduction
The physiologic and anatomic changes of pregnancy may result in development of
symptoms and signs that could be managed by educating and providing explanation.
1. Nausea and vomiting (morning sickness)
Some degree of nausea and vomiting during first trimester especially between the first and
the second missed periods is a very common complaint. It usually continues until about the
fourteen weeks of gestation. It can appear at any time of the day but is generally worse in the
morning, thus the name morning sickness. This condition is believed to be caused by high or
rapidly rising level of human chorionic gonadotrophic hormone and estrogen.
It is worse in multiple pregnancy and gestational trophoblastic diseases.
Psychological problems like anxiety can aggravate the situation.
Eating small feedings at more frequent intervals and avoiding food items whose smell
precipitate or aggravate the symptoms helps in relieving this problem. If persistent, anti-emetics
can be given.
2. Heartburn
Heartburn, epigastric burning sensation, is one of the most common complaints of pregnant
women especially during late pregnancy. The symptom is usually mild. It is caused by reflux
of gastric content into the lower esophagus due to upward displacement and compression of
the stomach by the enlarging uterus and progesterone induced relaxation of the lower
esophageal sphincter.
29

39. Obstetrics and Gynecology
It is relieved by having smaller meals, avoiding bending over or lying flat. Antacid
preparation (aluminum hydroxide or magnesium trisilicate alone orb in combination). In
severe cases H2 - blockers like cimetidine and ranitidine can be used safely.
3. Pica
Pica, craving of pregnant woman for items of low nutritional value like ice (pagophagia) or
clay (geophagia), can occur. No known cause has been identified but it is known to be
common in patients with iron deficiency anemia. In these cases, it is relieved by correction of
anemia. Some pregnant women may have the symptom with out anemia. Educating the
woman is all that is needed.
4. Ptyalism
Ptyalism, excessive salivation, is also common. It is not related to increased saliva
production; rather it is the result of reduced swallowing from nausea. Simple explanations
will suffice.
5. Constipation
Progesterone induced relaxation of smooth muscles and pressure by the uterus in the latter
part of pregnancy result in the common complaint of constipation. The problem is more
common with consumption of low fiber diet. This condition can be treated with high fiber diet
and increasing fluid intake. Sometimes bulk forming laxatives may be needed.
6. Hemorrhoids
Hemorrhoids, varicosities of the rectal veins, may first appear during pregnancy. More often
pregnancy causes exacerbation or recurrence of previous hemorrhoids due to increased
pressure in the rectal veins caused by obstruction of venous return by the large uterus.
Constipation during pregnancy also contributes for development of hemorrhoids.
Hemorrhoids can be asymptomatic or present with rectal bleeding, rectal pain or as a
prolapsed mass through the anal orifice. The later one can be strangulated and cause severe
pain. Thrombosis occurring in the dilated veins can also cause severe pain.
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40. Obstetrics and Gynecology
Treatment includes topically applied anesthetic and anti-inflammatory agents for pain and
swelling, warm soaks (sitz bath), laxatives and modification of bowel habits. Surgery is
reserved for thrombosed and strangulated hemorrhoids.
7. Urinary frequency
Increased glomerular filtration rate and in the latter part of pregnancy pressure by the
enlarging uterus explain the common complaint of frequency of urination. Urinary tract
infection is also common as the result of incomplete emptying of the bladder and stasis of
urine. Microscopy of urine must be done in all cases. Once UTI is ruled out simple
explanation is enough.
8. Vaginal discharge
Pregnant women normally develop increased vaginal discharge in many instances. It is
clear, whitish and odorless. This is the result of estrogen mediated increased mucus
secretion by the cervical glands. Reassurance is usually sufficient. If it is a cause of concern
vaginal douche with water mildly acidified with vinegar can be used. Vaginal infections like
trichomoniasis and candidiasis should be ruled out in every patient with this symptom.
Recurrent vulvo - vaginal candidiasis is common. Curd like vaginal discharge and vulvar
pruritis are major manifestations. Identification of Candida albicans by potassium hydroxide
stains confirms the diagnosis. Treatment with antifungal vaginal suppositories suffices.
Systemic antifungals are contraindicated.
.
9. Low Back and pelvic pain
Exaggerated lordosis and relaxation of the lumbar ligaments cause the common complaint of
low back pain. Minor degrees of pain may follow excessive strain or fatigue, bending, lifting
or walking. Its severity increases with the duration of pregnancy. Low back pain can be
reduced by having the woman squat rather than bending over when reaching down,
providing back support with a pillow when sitting down, and avoiding high heeled shoes.
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41. Obstetrics and Gynecology
Severe back pain with localized spinal tenderness should not be attributed simply to
pregnancy and further evaluation is needed.
Relaxation of the joints of the pelvic girdle, cause pelvic pain and gait abnormalities. In
severe cases there may be tenderness over the symphysis pubis which prevents mobility.
This condition is called pelvic osteoarthropathy and necessitates admission.
10. Varicose veins
Varicose veins, dilatation of the superficial veins of the lower extremities, could develop in
predisposed women. It becomes more prominent as pregnancy advances, weight increases,
and the length of time spent upright is prolonged. It is due to progesterone mediated smooth
muscle relaxation of the blood vessels and increased venous pressure in the femoral veins
due to compression by the enlarging uterus.
In most, it is asymptomatic. The only concern in these women is cosmetic. In few it causes
discomfort of variable degree.
Treatment is periodic rest with elevation of legs and use of elastic stocking or both. Surgical
corrections like injection of sclerosing agents, ligation and stripping are not generally
advisable during pregnancy.
11. Dependent edema
Edema of the lower extremities is common. It is as the result of increased venous pressure of
the lower extremities. It appears near the end of the day and disappears after a period of
rest.
It is important to rule out preeclampsia especially in those with persistent dependant edema.
12. Other complaints
Fatigue is the other common complaint during early pregnancy. The woman will have a
desire for excessive sleep. This symptom remits spontaneously by the fourth month of the
pregnancy and has no special significance.
Palpitation is another common complaint. If significant, cardiac pathologies must be ruled
out.
Chloasma and striae are other sources of concern for which no treatment is required. These
often regress but may not totally resolve after delivery.
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42. Obstetrics and Gynecology
Occasionally women complain about leg cramps. It is believed to be the result of
phosphorous deficiency and is relieved by dietary adjustment.
Parasthesia of the hands which usually occurs in the morning signify stretching of the roots
of the brachial plexus by drooping back of the shoulders in an attempt to maintain the center
of gravity.
Epistaxis and gum bleeding occur as the result of vascular congestion and do not need
special treatment. In rare cases surgical excision is needed for tumorous condition of the
gums called Epulis gravidarum.
Hyperemesis gravidarum
Severe nausea and repeated vomiting that precludes oral intake and leads to dehydration
and ketoacidosis is termed as hyperemesis gravidarum.
I. Pathophysiology
The cause is unknown but high levels of estrogen and HCG, vitamin B 6 deficiency and
psychologic factors are implicated. It is common in molar pregnancy, multiple pregnancy and
those with family or past history of this condition.
Because of starvation ketone bodies are formed from metabolism of fatty acid. Some of the
ketone bodies appear in the urine. In an attempt to restore the PH of the blood the
respiratory rate increases. Inadequate fluid intake results in dehydration, weight and reduced
urine output. Alkalosis from loss of gastric hydrochloric acid in the vomitus and hypokalemia
also develop.
II. Diagnosis
Presence of exaggerated nausea, excessive vomiting, weight loss and signs of dehydration
like fatigue, dry oral mucosa, weak pulse, low blood pressure and reduced urine are
hallmarks of this condition. Ketone in the urine confirms the diagnosis after exclusion of other
possible causes of excessive vomiting.
III. Differential diagnosis
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43. Obstetrics and Gynecology
Gastroenteritis, cholecystitis, hepatitis, pyelonephritis, intestinal parasitosis, peptic ulcer
disease and drug induced vomiting should be ruled out by history, physical examination and
laboratory investigations.
IV. Management
Once the diagnosis is confirmed the woman should be admitted after counseling of the
partners. The modalities include:
· Restricting oral intake
· Correcting dehydration and electrolyte deficit by intravenous crystalloid solution
preferably lactated ringer solution to maintain fluid balance
· Correcting acidosis by providing calories in the form of glucose in the intravenous
fluids
· Treating underlying causes by parenteral vitamin B 6 (if unavailable vitamin B
complex)
· Parenteral antiemetics like promethazine , chlorpromazine or metoclopramide
· Treatment of identified medical problems
· Monitor response to treatment by subjective feeling of the patient, weight, urine out
put and urine ketone determination
With clinical response, the patient can be started on oral feeding and antiemetics continued.
Therapeutic abortion is an option if the condition persists despite aggressive medical
treatment.
V. Complication
Prerenal azotemia, Mallory-Weis tears in the esophagus, in prolonged cases Werinkes
encephalopathy from thiamine deficiency.
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44. Obstetrics and Gynecology
Review Questions
1. Describe the measures that may be taken in a pregnant mother with nausea and
vomiting.
2. Discuss the possible causes of severe nausea and vomiting during pregnancy.
3. Describe important measures that may be taken in order to relieve the heartburn that
occurs during pregnancy in some mothers.
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45. Obstetrics and Gynecology
CHAPTER 5
ANTENATAL CARE (ANC)
Learning objective
· To discuss the contents of ANC, frequency and time of visit
· To describe the new WHO antenatal care model
· To enumerate high risk factors in pregnancy
Introduction-
Antenatal care (ANC) is a medical and general care that is provided to pregnant woman
during pregnancy. It is goal oriented with the aim of meeting both the psychological and
medical needs of pregnant woman with in the context of health care delivery system, culture
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46. Obstetrics and Gynecology
and religion in which the woman lives. ANC programs should be based on local situation and
should address risk assessment, health promotion and care provision. ANC has been found
to be effective in the treatment anemia, hypertension and sexually transmitted diseases.
Frequency and timing of visit
Traditional or standard (Western) model recommends the first visit to take place as early
as the first missed period. This allows accurate dating of the pregnancy and design
appropriate preventive and therapeutic interventions. Thereafter, subsequent visits are
planned every four weeks until 28 weeks, every two weeks between 28-36 weeks and every
week after 36 weeks. More frequent visits are required for high risk patients.
The new WHO ANC model recommends a minimum of four visits. It limits the number of
visits and restricts laboratory tests and procedures. First visit takes place at 16 weeks or
before. The second visit is planned between 24-28 weeks, the third at 32 weeks and the
fourth at 36- 38 weeks. The initial visit takes 30-40 minutes and the other visits take around
20 minutes each. Women with risk factors should not be enrolled in this model.
Activities of the new WHO ANC model
I. First visit at 16 weeks
Major activities are diagnosis of pregnancy and determination of the gestational age; risk
assessment and determination of the medical status of the mother; health promotion by
education on nutritional supplement, danger signs of pregnancy and finally care provision like
malaria prophylaxis, control MTCT of HIV, iron supplementation and immunization with
tetanus toxoid.
II. Second visit between 24- 28 weeks
Major activities are screening for hypertension, multiple gestation, anemia, preterm labor,
diabetes mellitus and RH sensitization; further health promotion and care provision and plan
birth place.
III. Third visit at 32 weeks
Major activities are screening for hypertension, anemia, multiple pregnancy, diabetes mellitus
and RH sensitization; health promotion and care provision and plan birth place.
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47. Obstetrics and Gynecology
IV. Fourth visit at 36 weeks
Major activities are screening for hypertension, antepartum hemorrhage, multiple gestations;
check for fetal lie, presentation, growth and well being; health promotion and care provision
and finally up date individualized birth plan.
Contents of ANC visit
I. Assessment
Detailed history and physical examination (refer to chapter 2) along with necessary
laboratory investigations should be done in the initial visit to assess the general medical
status of the woman and pick risk factors. For this reason the initial visit takes 30-40 minutes.
Subsequent visits look into new developments, therefore, take much shorter time.
A. Initial visit
The pertinent elements of the history during the initial visit include
1. History of present Pregnancy- identification (name, age, address, marital status,
occupation); pregnancy facts (planned or unplanned pregnancy, wanted or unwanted,
supported or unsupported); gravidity , parity, abortion, LMP, gestational age,
contraceptive use prior to pregnancy, symptoms and signs of pregnancy , danger signs
and symptoms, fetal quickening , client concern or complaints
2. Past history - antepartum and postpartum hemorrhage, multiple pregnancy,
preeclampsia, eclampsia, sepsis, sexually transmitted infections, operative deliveries, still
birth and neonatal death, preterm delivery, low birth weight baby, chronic medical
illnesses (hypertension, diabetes, drug allergy and cardiac diseases) and surgical
problems, genital mutilation
3. Others- personal, social and family history
General physical examination as described in chapter 2 should be performed. It includes the
general appearance, vital signs, weight and height, general systemic examination including
checking for signs of anemia, physical abuse and surgical scars. Specific obstetric
examination should focus on determining the uterine size, fetal lie and presentation, fetal
growth and well being, fetal heart beat. Pelvic assessment is performed upon indications.
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48. Obstetrics and Gynecology
In the standard model baseline laboratory investigations are hemtocrite, blood group and
Rhesus factor, urinalysis (protein, ketone and microscopy), VDRL and stool examination for
ova and parasites. Others that could be done upon indication or when resources permit are
pap smear, cervical /vaginal smear, urine culture and sensitivity, complete blood count,
pregnancy test, serology for HIV, hepatitis b virus and TORCH screening, oral glucose
tolerance test, maternal serum alpha fetoprotein on 16 weeks, amniocentesis
,ultrasonography and others.
In the new WHO model urine dip stick for bacteria and protein, VDRL and blood group and
Rhesus factor determination are only done in the first visit. Hemtocrite is only done if there
are clinical signs of anemia.
In the new WHO model, in the initial visit women are grouped into two using the classifying
form. Women with out any risk factor are enrolled in the basic component of the new model
that needs only three visits till delivery. Women with any identified risk factor need special
care that may need frequent visits or even referral for specialized care.
The classifying form has 18 components that are grouped into three:
· Obstetric history- previous stillbirth/ neonatal loss, history of three or more
consecutive abortions, birth weight of less than 2500 or more than 400 grams,
admission in the last pregnancy for preeclampsia or hypertension, previous uterine or
cervical surgery-
· Current pregnancy - diagnosed or suspected multiple pregnancy, age less than 16
or more than 40, RH isoimmunization, vaginal bleeding, pelvic mass, diastolic blood
pressure of more than 90 mmhg
· General medical condition- insulin dependent diabetes mellitus, renal or cardiac
disease, known substance abuse, any other severe medical illness
B. Subsequent visits
History focuses on new complaints and problems since the last visit, intercurrent illnesses
and medications, quickening time and fetal movement, danger symptoms of pregnancy and
any changes in the personal history of the woman.
Physical examination focuses on the general appearance, vital signs mainly the blood
pressure, weight, checking for signs of anemia, fundal height, fetal lie and presentation, fetal
heart beat, leg edema and other examinations based on the complaints.
39

49. Obstetrics and Gynecology
In the standard model hemtocrite is done at 24-28 and 32 weeks, antibody screening and
oral glucose tolerance test at 28 weeks, ultrasound and maternal alpha feto protein at 16
weeks and fetal survellance tests starting 32 weeks.
In the new WHO model dipstick of urine for bacteria is done in all visits. Urine dipstick for
protein is only done for nulliparous women or for those with history of preeclampsia or
hypertension currently. Hemtocrite is done at the third visit.
II. Health promotion (advice and counseling)
Advice the woman about the importance of balanced diet and avoidance of drugs, smoking
and alcohol: adequate rest; hygiene and safe sex.
Discuss about minor complaints of pregnancy and the danger symptoms of pregnancy.
Discuss about whom to contact and where to go if these symptoms develop.
Inform the woman to record the time of quickening. Education about labor and preparation
for labor/ delivery should be done starting from the third visit. The need for clean and safe
delivery should be stressed. Breast feeding and family planning after delivery should be
discussed.
III. Care provision (care provided)
Individualized delivery plan in should be planned starting from the first visit and continued
during subsequent visits including arrangement of transportation in cases of emergency.
Place of birth and who attends birth should be planned.
Universal ferrous sulfate prophylaxis for nutritional anemia should be given starting from the
first visit. Tetanus toxoid vaccination should be given according to WHO guidelines.
Appropriate prophylaxis and treatment of intestinal parasites and malaria should be offered.
Where indicated antiretroviral therapy should be offered to HIV positive pregnant women.
Appropriate management of complaints and identified problems/ complications should be
done in each visit.
Timing and importance of next visit should be discussed. Appointment should then be
scheduled.
High risk factors (not inclusive)
I. Past obstetric history
· Ectopic pregnancy and recurrent spontaneous abortion
· Multiple pregnancy or preterm labor
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50. Obstetrics and Gynecology
· Antepartum or postpartum hemorrhage
· Malpresentation
· Intrauterine fetal death, stillbirth or early neonatal death
· Birth weight of less than 2500 or greater than 4000 grams
· Difficult operative deliveries and caesarian section
II. Present obstetric history
· Short stature (height of less than 150 cm), age of less than 16 or greater than 40
· Primigravida or grandmultiparity
· Vaginal bleeding at any gestational age
· Uterine size to gestational age discrepancy (big or small for date uterus)
· Multiple gestation
· Premature rupture of the membranes
· Raised blood pressure during pregnancy
· Malpresentation after 34- 36 weeks
· Unwanted pregnancy
· Extreme social disruption and deprivation
Review questions
1. Briefly describe the new WHO ANC model.
2. List the routine laboratory investigations in ANC.
3. List the high risk factors in pregnancy.
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51. Obstetrics and Gynecology
CHAPTER 6
ABNORMAL BLEEDING DURING FIRST AND SECOND TRIMESTERS OF PREGNANCY
Learning objectives
· To identify the common causes of abnormal bleeding during pregnancy by trimester.
· To list the different types of abortion with their clinical features.
· To describe the clinical feature of ectopic pregnancy.
· To describe the management the different types of abortion and ectopic pregnancy.
· To define the spectrum of GTD
· To discuss the clinical features of GTD
42

52. Obstetrics and Gynecology
· To list the main treatment modalities of GTD
· To enumerate the possible complications GTD and their treatment
Introduction
When a woman becomes pregnant, the menstrual bleeding stops until sometime after the
end of the pregnancy. However, abnormal bleeding from the genital tract can complicate
some pregnancies. Statistically, more than 25% of all gestations will present to health care
provider at least in early pregnancy with vaginal bleeding and/or pelvic pain. These
symptoms may indicate a minor or a life threatening condition that can result in death.
Successful management of any one of these conditions is of paramount importance and
rests on timely diagnosis. This in turn requires proper evaluation of the patient by taking the
history and doing physical examination. There may be a need to do some laboratory studies
to help the evaluation process. The primary goal of the evaluation should focus on identifying
immediate life threatening conditions like shock. Generally, abnormal uterine bleeding during
pregnancy can result from obstetric or non-obstetric causes. Conditions like abortion, ectopic
pregnancy, placenta abnormalities like placenta previa and abruptio placentae, and
gestational trophoblastic diseases are some of the obstetric causes. While conditions like
genital infections, trauma to the genital organs and neoplastic changes affecting them are
some of the non-obstetric causes. Systemic illnesses affecting blood coagulation can also
result in abnormal bleeding during pregnancy.
1. ABORTION
1.1. Importance
Abortion is an important cause of bleeding during pregnancy, as it is one of the five leading
causes of maternal death in the developing world. The other causes being obstructed labor,
hypertensive disorders of pregnancy, hemorrhage and infection.
1.2. Definition:
Abortion is the expulsion of the fetus from the uterus or termination of pregnancy before fetal
viability. This is usually taken to be so if it happens before 28 completed weeks of gestation
or less than 1000g weight in Ethiopia & United Kingdom.
1.3. Classification
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53. Obstetrics and Gynecology
1.3.1. By occurrence
Abortion could occur spontaneously or could be induced.
A. Spontaneous abortion
An abortion is said to be spontaneous if it occurs with no intervention. The incidence of
spontaneous abortion is between 10% and 20% of all pregnancies. It is most commonly due
to fetal chromosomal defects such as trisomies, monosomies and polyploidy. This usually
occurs during the first trimester.
B .Induced abortion
An abortion is said to be induced if it results from medical or surgical intervention that can
cause abortion. It could be safe or unsafe abortion. Unsafe abortion characterized by lack or
inadequacy of skill of provider, hazardous technique and unsanitary facilities or both. This is
important type of abortion as it accounts for the major proportion of abortion and is cause of
immense maternal mortality and morbidity. Moreover, it is related to unwanted pregnancy
and unawareness of the reproductive physiology by the woman .It can largely be prevented if
there is provision of contraceptive service and making the woman knowledgeable about her
reproductive physiology. Of the 210 million pregnancies that occur each year, about 46
million (22 per cent) end in abortion. About 20 million of those abortions are unsafe –that is,
performed by someone without the skills or training to perform them safely, or in a place that
does not meet minimal medical standards or, both. Every year, more than 70,000 women die
as a result of unsafe abortion; hundred of thousands more suffer from serious, often
permanent, disabilities. Everyday, 200 women die from unsafe abortion. More than 95% of
deaths and injuries occur in developing countries. In Ethiopia maternal losses from abortion
and its complication account for 25-50%. The majority of deaths from abortion result from
hemorrhagic shock and sepsis. Proper management of abortion can prevent the death and
the other complications that result from it.
C.Therapeutic abortion
Subset of safe abortion which is performed for the purpose of saving the life of the mother (3)
or if the fetus has congenital / chromosomal / metabolic disorders that is incompatible with
life after birth.
1.3.2. By clinical stages
Threatened abortion: is a clinical condition that is characterized by vaginal bleeding before
28 weeks of gestation. In addition there is crampy lower abdominal pain and the cervix
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54. Obstetrics and Gynecology
remains closed. The fetus is alive and there is a chance of continuing the pregnancy to
viability.
Inevitable abortion: is a clinical condition characterized by vaginal bleeding of variable
amount and crampy lower abdominal pain. The cervix is open but no products of conception
have been expelled. There is no chance of salvaging the pregnancy.
Incomplete abortion: is a clinical condition in which vaginal bleeding continues and cervix
remains open despite expulsion of part of the products of conception.
Complete abortion: is a clinical condition in which vaginal bleeding stops and the cervix
closes following expulsion of all products of conception. The uterus is small for the duration
of the pregnancy and it is firmer. Before 14-16 weeks it is difficult to tell if an abortion is
complete or not because to make sure it is complete one has to identify the fetus and the
placenta with the membranes as fully formed structures. Before 14-16 weeks these
structures are not sufficiently well formed.
Missed abortion: is a clinical condition in which the fetus dies in utero and is retained for at
least four weeks. There is usually history of threatened abortion preceding it. Decidual
necrosis may result in brownish vaginal discharge. Pregnancy symptoms like morning
sickness, breast tenderness and abdominal girth increment disappear. Cessation of fetal
movement is reported by the mother if it occurs after 18 weeks. Failure of uterine growth
results in small for gestational age uterus. Pregnancy test takes 8 weeks to become
negative.
1.3.3. By associated infection
Septic abortion: is a clinical condition in which offensive vaginal discharge, temperature of
more than 38 o centigrade and lower abdominal pain / tenderness accompany any of the
clinical stages of abortion. Majority follow unsafely induced abortions. Infection starts in the
uterus and if untreated spreads to adjacent pelvic organs (pelvic peritonitis) or to the general
peritoneum (generalized peritonitis) or the blood stream (sepsis). It eventually results in
death by causing septic shock.
Postabortal sepsis: is pelvic infection after a complete abortion.
1.3.4. Other definitions
Recurrent abortion: occurrence of three or more consecutive spontaneous abortions. It was
previously known as habitual abortion.
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55. Obstetrics and Gynecology
1.4. Initial assessment
Any woman of reproductive age experiencing at least two of the following symptoms should
be considered as a possible abortion patient.
· Vaginal bleeding
· Cramping and/or lower abdominal pain
· A possible history of amenorrhea
Complete clinical assessment is necessary to determine all conditions that are present in
order to decide the order in which to treat them.
1.4.1. History
· Length of amenorrhea
· Bleeding (duration, amount)
· Cramping (duration and severity)
· Abdominal or shoulder pain
· Drug allergy
· History of interference and method employed
· Symptoms of infection
1.4.2. Physical examination
· Check vital signs
· Note general health of the women
· General systemic examination
· Abdominal examination
Check –abdominal distension, movement with respiration, bowel
sound,
Location and severity of tenderness and rebound tenderness,
Uterine size, masses, shifting dullness
· Pelvic examination(speculum and bimanual digital examination)
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56. Obstetrics and Gynecology
Remove any visible products of conception from the vaginal canal or cervical canal.
Then note for the amount of bleeding and presence of offensive discharge, the extent
of cervical dilation and presence of cervical excitation tenderness, size and consistency
of the uterus, adenexal masse and other pelvic masses. Check for cervical laceration
1.4.3. Laboratory examination
Based on clinical assessment when indicated: -
· hemoglobin / hemtocrite, blood group and rhesus factor
· white cell count, erythrocyte sedimentation rate, urinalysis, renal function test, liver
function test, platelet count, prothrombin time, partial thromboplastin time
· Plain film of the abdomen (erect), pelvic ultrasonography
· Pregnancy test
1.5. Management
Life threatening conditions like shock (hypovolumic or septic), severe anemia and sepsis
should be treated aggressively prior to instituting specific treatment. These include
intravenous fluids, parenteral antibiotics, blood transfusion and /or other ventilatory supports.
Preparations for laparatomy must be made in cases suspected or diagnosed to have uterine
perforation or generalized peritonitis or pelvic abscess. Specific management for each stage
of abortion should be offered only after attending to the above conditions. Appropriate and
timely referrals are life saving.
1.5.1. Threatened abortion
· Bed rest at home which could be reinforced by sedatives like diazepam. Women who
have bled much (regardless of the gestational age) or have bad obstetric history or
live far away and cannot get help if bleeding becomes much worse, especially during
the night should be admitted for observation.
· Avoid intercourse and douching
· Monitor progress by subsequent assessment. Where available ultrasonography
should be done to check for viability.
· If there is any sign of pelvic infection evacuation of the uterus should be performed.
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57. Obstetrics and Gynecology
1.5.2. Complete abortion
If completeness is confirmed either by examination of the conceptus tissue or
where available by ultrasound
· Administer ergometrine 0.5mg
· If justified provide therapeutic or prophylactic antibiotics
Evacuation of the uterus must be done if completeness can not be assured as
in early abortion or expulsion occurred out of the health institution.
1.5.3. Inevitable abortions
A. Less than 14 weeks of gestation:
Evacuation of the uterus is the mainline of treatment .Evacuation can be done
either by sharp metallic curettage or by manual vacuum aspirator (MVA). MVA is
much safer and recent technology which is said to be associated with less
complications and pain, more efficient in evacuating the uterus in less time and
thus can safely be used by lower level health professionals.
Mandatory indications for evacuation
1. Considerable bleeding
2. Bleeding which continues for more than 24 hours.
3. Patients in whom the retained products of conception are obviously still
present on vaginal examination..
B. More than 14 weeks of gestation
In the absence of heavy bleeding evacuation of the uterus is not advised before the
expulsion of the fetus .Management includes
· Admission and monitoring the vital signs and the amount of bleeding
· Once the fetus / placenta are expelled completeness should be checked
.Evacuation of the uterus must be done if incomplete or the bleeding
continues.
· Ergometrine or oxytocin as drip should be given for continued bleeding after
expulsion or evacuation and monitoring should continue.
· Exploration of the uterus for remnants or perforation should be done if these
measures fail and the patient continues to bleed.
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58. Obstetrics and Gynecology
1.5.4. Incomplete abortion
Uterine evacuation should be done preferably by MVA. Antibiotics as needed can be
given.
Methods of Uterine evacuation
Determined by uterine size
If uterine size < 14 weeks
· Manual / electrical vacuum aspiration or evacuation and
curettage(E&C)/dilatation and curettage (D&C)if cervix is closed
If uterine size > 14 weeks
· Oxytocin infusion or evacuation and curettage(E&C)/dilatation and
curettage when appropriate
Oxytocin administration
Add 10ml (ampoules) to 1000ml lactated Ringer's solution (100mu/ml)
Start at 0.5ml/mi (50mu/mi), increase at 30 to 40min intervals up to a maximum rate
of 2mml/mi (200mu/min). If effective contractions are not established at this infusion
rate, increase the concentration. Discard all but 500ml of the remaining solution. Add
additional 5 ampoules of oxytocin (200mu/ml). Reduce the rate to 1ml/mi (200mu/mi).
Increase up to 2ml/mi (400mu/mi), continue at this rate for 4-5hrs or until fetus is
expelled.
1.5.5. Missed abortion
A. Expectant management up to 4 weeks
· This is based on the fact that 95% women with missed abortion will abort
spontaneously in 4 weeks time, whatever the duration of the pregnancy. After 4
weeks the chance of developing disseminated intravascular coagulation or dead
baby syndrome is significant.
· During this time coagulation profile is monitored weekly. Evacuation of the uterus
is done if the patient did not expel in 4 weeks or before 4 weeks if coagulation
derangement occurs.
B. Aggressive management
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59. Obstetrics and Gynecology
This entails evacuation of the uterus. Methods include dilatation and curettage
(D&C) for uterine sizes up to 12 weeks or induction of labor by prostaglandins
/oxytocin infusion if uterine size is more than 12 weeks. Since there is a risk of
uterine perforation and coagulopathy with this form of management appropriate
referral to proper health facility should be made.
1.5.6. Management of Complications
I. Uterine perforation
The following signs seen during uterine evacuation indicate perforation.
· An instrument (sound, cannula, and curette) extends beyond the expected
limit of the uterus.
· Fat or bowel is found in the tissue removed from the uterus
· Severe pain and continuous bright red bleeding
· In apparent vital sign derangement (hypotension in the absence of bleeding)
Management
· Stabilize the patient and do not give anything per os.
· Monitor vital signs
· Start broad spectrum antibiotics (parenteral)
· Immediate referral to a facility capable of performing gynecologic surgeries.
If evacuation is complete
· Give ergometrine 0.5mg
· Observe her for two hours
· If patient become stable and bleeding stops, give ergometrine and
continue observation overnight
· If the condition gets worse and the bleeding doesn’t stop
emergency laparatomy is performed.
If evacuation is not complete
· Immediate laparatomy to complete evacuation under direct vision Depending
on the findings either repair or hysterectomy is done.
II. Intraabdominal injury
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60. Obstetrics and Gynecology
The following signs and symptoms indicate intra abdominal injury
Symptoms
· Nausea, vomiting, shoulder pain,fever,abdominal pain and cramping
Signs
· Distended abdomen, decreased bowel sound, tense hard abdomen
· Rebound tenderness
Management
· Resuscitation, parenteral antibiotics,
· Immediate referral for laparatomy
III. Sepsis
Etiology is polymicrobial (gram positives, gram negatives and anaerobes)
The following symptoms and signs indicate that either local or generalized infection is
likely:
Symptoms
· Chills, fever, sweating, history of interference
· Prolonged bleeding, general discomfort, flu like symptoms
Signs
· Foul smelling vaginal discharge, distended abdomen
· Tenderness, low blood pressure
Assess women’s risk for developing septic shock
Low risk
· First trimester abortion, mild to moderate fever (< 38.50 c)
· Stable vital signs, no evidence of Intraabdominal injury
High risk
· second trimester abortion, high fever (> 38.50 c)
· Any evidence of intra abdominal injury, shock
Management
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61. Obstetrics and Gynecology
· Resuscitation, monitor vital signs, start broad spectrum antibiotics
intravenously
If low risk and stable
Uterine evacuation, continue antibiotics, observe for 48 hrs.
If high risk
· Continue antibiotics
· If there is shock ---- manage as shock
· If intra abdominal injury--- laparatomy
· If DIC present -- treat with clotting factors and fresh blood products
IV. Other complications and their management
· Anemia - manage according to severity by either hemathenics or blood
transfusion
· Renal failure - manage accordingly
· Give tetanus toxoid as indicated and tetanus antitoxin for non immune women
· Give anti-D for Rh negative mothers (see protocol for management of Rh
isoimmunization)
1.5.7. Post abortion family planning
All women receiving post abortion care need counseling and information to ensure
that they understand:
· They can become pregnant again before the next menses
· There are safe methods to prevent or delay pregnancy
· Where and how they can obtain family planning service
1.5.8. Antibiotic choices and administration in the management of abortion
Empiric therapy antibiotic covering wide variety of aerobic, anaerobic, gram
negative/positive organisms is used.
Regimen 1
Ampicillin or benzyl penicillin plus chloramphenicol or clindamycin or metronidazole
plus gentamycin
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62. Obstetrics and Gynecology
Regimen 2
Ceftriaxone or ciprofloxacin plus gentamycin or metronidazole
Regimen 3
Doxycycline with metronidazole
· Once started, therapy can be continued until the patient is afebrile at least for 24
hours, preferably 48 hours
· If there is no response in 48 hours the antibiotics should be changed and/or
complications considered
· When recovery is underway, intravenous therapy should be followed by oral
medication, for 10 to 14 days.
1.5.9. Components of Post abortion care (PAC)
· Emergency treatment of incomplete abortion and potentially life threatening
complications
· Post-abortion family planning counseling and services
· Links between post-abortion emergency services and the reproductive health care
system.
· Community service provider partnership
· Counseling
2. ECTOPIC PREGNANCY
2.1. Definition
Ectopic pregnancy is implantation of the fertilized ovum outside of the uterine endometrial
cavity.
2.2. Incidence and predisposing factors
Ninety–nine percent of ectopic pregnancy occurs in the fallopian tube. The commonest site is
the ampulla which accounts for 55% of ectopics. The rest occurs in the isthmus (25%), the
fimbria (17%) and the interstitial part (2.5%). Rare forms of ectopic pregnancy include
cervical ectopic, ovarian ectopic and abdominal pregnancy. Very rarely bilateral ectopic or
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63. Obstetrics and Gynecology
combined intrauterine and ectopic pregnancy is seen. In many parts of the world one in every
50 to 200 pregnancies is ectopic.
Any condition that alters the length, contour, peristaltic movement or size of the tubal lumen
will predispose to ectopic gestation. Common conditions that predispose to ectopic gestation
are:
· Previous gonococcal or Chlamydia endosapingitis
· Postoperative like previous ectopic surgery/tuboplasty or inflammatory pelvic
adhesions distorting the tubes
· Congenital abnormalities of the tubes
· Some family planning methods like progestasert and progesterone only pills
· Medically assisted conception
2.3. Natural Coarse of tubal ectopic pregnancy
Majority of ectopic gestations end as gynecological/obstetric emergencies in the first or early
second trimester. It is a very rare occurrence for an ectopic gestation to advance to term. As
the fertilized ovum grows, it progressively distends the tube which leads to unilateral lower
abdominal pain. Further distension eventually leads to either rupture into the lumen (tubal
abortion) or more commonly into the peritoneal cavity (tubal rupture). This results in extrusion
and death of the zygote accompanied by intraperitoneal bleeding from the edges of the
ruptured tube. For isthmic ectopic this occurs 3-4 weeks from the LMP while in ampullary it is
around 6-8 weeks and in interstitial it is around 12 weeks. Unless surgical intervention is
undertaken majority of patients die of massive intraperitoneal bleeding. Rarely an abdominal
pregnancy results if the zygote survives and implants in the peritoneal cavity.
Sometimes chronic ectopic gestation results if pelvic adhesions limit the extent of the
bleeding forming a pelvic mass. .
2.4. Clinical features and diagnosis
The clinical features are often atypical and diverse especially before rupture. As it is one of
the most devastating and potentially fatal gynecologic emergencies, every clinician should be
suspicious of it all the time. The adage ’any woman of child-bearing age (15-50) who has
abdominal pain (with or without amenorrhea) may have an ectopic gestation unless proven
otherwise’ is a useful one to bear in mind.
Typically women present with the three triad of symptoms – variable period of missed
menstrual period, abnormal vaginal bleeding and lower abdominal pain. Commonly there is a
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64. Obstetrics and Gynecology
short period of missed period but in some women the vaginal bleeding may coincide or even
precede the expected time of menses. The vaginal bleeding is often dark red and small in
amount with heavy bleeding being a rarity. Sometimes passage of decidual cast may
confuse the diagnosis with abortion. The lower abdominal pain is initially unilateral and
constant in nature but after tubal rupture it becomes diffuse. Syncopal attack may be
reported at the time of rupture. With significant hemoperitoneum shoulder pain and rectal
fullness may be reported. Presence of predisposing factors should be sought. High grade
fever is unusual.
Physical signs are also variable and largely depend on the presence or absence of rupture.
Vital signs may range from normal to profound shock. Pallor is also variable. Peritoneal
irritation (direct tenderness/rebound tenderness/guarding) of variable degree is always
present, which could be localized to the lower abdomen or diffuse. Shifting dullness indicates
hemoperitoneum.
The most significant findings on pelvic examination include closed cervix with positive
cervical excitation tenderness, unilateral adenexal tenderness with or without tender mass
and tense/tender pouch of Douglas. Uterine enlargement up to 8 weeks size is a normal
finding.
The most valuable bedside diagnostic procedure for ruptured ectopic pregnancy is
culdocentesis.This involves aspirating fluid from the pouch of Douglas by passing needle
through the posterior fornix. Finding dark red non clotting blood is invariably diagnostic.
Negative culdocentesis does not rule out ectopic pregnancy.
Laboratory investigations (where available) that could help in the diagnosis of unruptured
ectopic include Serum b HCG determination in conjunction with pelvic ultrasound.
2.5. Management
The treatment can be medical or surgical depending on the type of the ectopic pregnancy.
The best management for ruptured ectopic is emergency laparatomy to ligate the bleeding
vessels coupled with aggressive resuscitation to counteract the effects of hypovolemia.
Timely referrals to a hospital setting with continued resuscitation along the way is life saving.
Unruptured ectopic is usually managed using drugs like methotraxate or conservative tubal
surgery.
Resuscitation
· Correcting hypovolemia with intravenous fluid
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65. Obstetrics and Gynecology
· Blood transfusion before operation; this may in fact be undesirable if it delays very
urgent surgery to stop bleeding.
Surgical treatment- Salpigectomy /sapingeo-oophoerctomy
Upon discharge women should be counseled about the risk of recurrence in future
pregnancy and the importance of visiting a clinician as soon as they miss their menses.
3. GESTATIONAL TROPHOBLASTIC DISEASES (NEOPLASMS)
3.1. Definition
Pregnancy-related pathological conditions in which there is abnormal growth and
development of the trophoblast. GTDs include the tumor spectrum of hydatidiform mole,
invasive mole or chorioadenoma destruens, and choriocarcinoma.
3.2. Classification
There are various schemes of classification, but the following is a commonly used one:
1. Benign GTD includes hydatidiform mole (complete and partial).
2. Malignant GTD falls into two groups:
a. Non-metastatic includes persistent hydatidiform mole, invasive mole and
choriocarcinoma which has not metastasized.
b. Metastatic includes metastatic mole and choriocarcinoma.
3.3. Unique Features
Gestational trophoblastic diseases have a number of unique characteristics:
· They consist of tissue “foreign” to the patient. They arise from the fetal tissue in the
maternal host.
· They secrete an accurate and sensitive tumor marker, the human chorionic
gonadotrophic hormone (HCG).
· They are markedly sensitive to chemotherapy so that even advanced disease may be
cured.
· Unlike other epithelial tumors malignant GTDs spread mainly by vascular route.
· Normal pregnancies are possible following molar pregnancy.
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66. Obstetrics and Gynecology
3.4. Benign GTDs (Hydatidiform mole)
3.4.1. Types of molar pregnancy
A. Complete mole
Uterus is filled with multiple grapes like vesicles. There is no fetus or amnion.
Microscopically, there is pronounced and generalized hydropic swelling and edema of
villous stroma, avascular villi and marked proliferation of syncitiotrophoblastic and
cytotrophoblastic elements surrounding the villi. The incidence of postmolar GTD is 15
to25 % (17 % is non metastatic type).
B. Partial or Incomplete mole
An abnormal fetus or embryo is present, but it usually dies in the first trimester. Focal
vesicles are seen. Microscopic features include localized hydropic villi and trophoblastic
proliferation along with presence of fetal tissue, and blood vessels. Post molar GTD
develop in 5 to 10 % of patients (almost always of non metastatic type).
3.4.2. Incidence and risk factors
Hydatidiform mole (molar or vesicular pregnancy) is the most common form of GTD.
Incidence is very variable ranging from 1:200 – 1:300 in South East Asia to 1:1500-1:2000
in U.S.A. Risk factors include:
· Age less than 20 or more than 40 years
· Genetic factors
· Low socioeconomic status
· Protein, folic acid and carotene deficiency
· Previous molar pregnancy (recurrence rate is around 1:76 for the first and
1:6 for the second)
3.4.3. Clinical features
· Vaginal bleeding after a period of amenorrhea (usually starting from the first
trimester)
· Serosangineous vaginal discharge
· Passage of the “grape-like” vesicles, if occurs, is considered to be
pathognomonic.
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67. Obstetrics and Gynecology
· Exaggerated symptoms and signs of pregnancy mainly hyperemesis
gravidarum
· Pre-eclampsia occurring before the gestational age of 20-24 weeks is seen in
around 30% of patients
· The uterus will be big-for-date in half of patients but small-for-date in a third
and appropriate for gestational age in the rest.
· The uterus is doughy with no fetal parts felt except in the situation of partial
mole.
· FHR tones are absent except partial mole.
· The ovaries may be palpably enlarged by the theca lutein cysts.
· One may also find clinical and/or biochemical signs of hyperthyroidism due to
the elaboration of thyrotropin by the tumor or as the effect of elevated HCG.
3.4.4. Diagnosis
.Whenever molar pregnancy is suspected on clinical grounds the patient should be
referred to an appropriately equipped facility for confirmation of the diagnosis and
management. The most important investigations that help in the diagnosis are
determination of serum or urinary B-HCG in titer
which reveal very high values and ultrasonography which reveal the typical snow- storm
appearance without gestational sac or fetus. Other modalities like amniography which
shows the honey comb pattern are no more used.
3.4.5. Complications of molar pregnancy
Medical complications include anemia and shock from hemorrhage, pre-eclampsia,
hyperemesis gravidarum, hyperthyroidism and intrauterine infection with or without
sepsis. Congestive heart failure and pulmonary edema could result from trophoblastic
deportation, fluid overload during treatment or from pre-eclampsia / severe anemia/
hyperthyroidism. Trophoblastic deportation may result in acute respiratory distress within
6-8 hours of evacuation.
Post molar GTD and future recurrence other problems. Uterine perforation could result
during treatment. There may be deposition of trophoblast in the lungs but spontaneous
regression occurs.
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68. Obstetrics and Gynecology
3.4.6. Management
Since molar pregnancy is associated with many disease and treatment related
complications, its management should be in a facility that is capable of handling them.
Furthermore prolonged follow up is needed for early detection and management of post
molar GTD. For these reasons timely referral from the health center is crucial.
Management in an appropriate setting includes
· Performing baseline investigations – B-HCG level, chest X-ray, liver and renal
function tests and complete blood count.
· Treatment of medical complications
· Evacuation of the molar tissue. The method of choice is suction curettage.
Medical induction by uterotonic drugs is not favored because it carries risk of
hemorrhage and embolization. Hysterectomy with mole in situ is the preferred
treatment for women having more than three children and /or women older than
40 years. Sharp metallic curettage is contraindicated.
· Follow up using history, physical examination and B-HCG titer done weekly until it
is negative three times then monthly for one year. Combined oral contraceptives
are given during this period to prevent pregnancy.
· Platueing or rising HCG levels , rising levels after negative HCG ,HCG still high
after 6 months of evacuation and any clinical sign of metastasis are indicative of
post molar GTD and require chemotherapy.
3.5. Malignant GTDs
3.5.1. General
These are mainly invasive mole and choriocarcinoma.
A. Invasive mole makes up around 15% of GTN and is reported in 10-15 % of patients
who have had primary molar pregnancy. It invades the myometrium and the uterine
vessels extensively; therefore, the diagnosis is usually made from pathologic examination
of hysterectomy specimens.
B.Choriocarcinoma is rare, making up only 2-5% of all cases of GTD and follows 2-10%
of molar pregnancy. It is an aggressive fast-growing tumor with disordered trophoblastic
proliferation, myometrial invasion, hypervascularity, necrosis and hemorrhage, the
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69. Obstetrics and Gynecology
absence of villous structures and metastases. 50% follow hydatidiform mole. A quarter
follow term pregnancies and another quarter follow abortion or ectopic pregnancy. It
spreads both by local invasion and via vascular route which occurs early. Common sites
of metastasis are the lungs (80%), anterior vaginal wall (30%), the brain (10%) and the
liver (10%). All GTDs that follow normal pregnancy are choriocarcinoma.
3.5.2. Clinical Features
· Severe vaginal bleeding which may be absent in some cases.
· Fulminant pre-eclampsia and hyperthyroidism
· Metastases may occur to the lungs, liver, brain, vagina, gastrointestinal tract,
and bones and may manifest as follows:
· Pulmonary metastasis with cough, chest pain, hemoptysis
· Liver secondary with abdominal pain, hepatomegally,
jaundice
· Brain metastasis with headache, convulsion, focal neourologic
deficit
· Vaginal metastasis with a bleeding blue-purple vaginal
mass
· GI metastasis with hematemesis, melena, hematochezia
· Bone metastasis with pain, pathological fractures
3.5.3. Diagnosis
Finding elevated B- HCG levels along with pathologic identification of typical lesions
confirms the diagnosis. Chest and bone X-rays, cerebrospinal fluid analysis and
ultrasound may help in identifying metastasis.
3.5.4. Management
This is best if done in specialized centers or at least in centers where the appropriate
investigations can be done and the patient can receive the right treatment. The
management modality is single or combination chemotherapy. Surgical removal of
persistent cases is a secondary option.
3.6. Long-term sequelae
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70. Obstetrics and Gynecology
The prognosis is always excellent for hydatidiform mole. Also, almost all patients with
malignant non-metastatic GTD are cured with appropriate therapy .Recurrence, when it
occurs, is usually in the first several months of termination of therapy but may sometimes
occur as late as 3 years or more. There is high risk of recurrence of GTD in future
pregnancies. The effect on the subsequent fertility of young patients is insignificant. But
because of the slightly increased risk of choriocarcinoma, B-HCG should be determined
at 3 week and 3 months following delivery.
Review Questions:
1. Define unsafe abortion and recurrent abortion
2. Describe the clinical stages of abortion with respect to bleeding, cervical status,
uterine size and other signs.
3. Outline the management of incomplete abortion and septic abortion.
4. List the methods of uterine evacuation for uterine size less than 14 weeks.
5. Discuss the essential components of post-abortion care.
6. Discuss the clinical features of ectopic pregnancy.
7. Describe culdocentesis.
8. Describe the spectrum of gestational trophoblastic diseases.
9. Discuss the most important clinical features of molar pregnancy.
10. Describe how molar pregnancy is managed and also discuss how post-evacuation
follow-up is undertaken.
CHAPTER 7
ANTEPARTUM HEMORRHAGE
Learning Objectives
· To identify the major causes of ante partum hemorrhage
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71. Obstetrics and Gynecology
· To list important risk factors for ante partum hemorrhage
· To discuss the evaluation of a patient with antepartum hemorrhage
· To indicate the important precautions that should be taken in evaluating and
managing mothers with antepartum hemorrhage
· To explain the basic principles of the management of antepartum hemorrhage
Introduction
Antepartum Hemorrhage (APH) is bleeding from the genital tract of the pregnant mother after
the fetus has reached the age of viability (which is after 28 completed weeks or fetal weight
of 1000gm or more) and before the fetus is delivered. It occurs in 2-4% of all pregnancies.
The causes could broadly be grouped into two.
· Obstetric causes which include placenta previa, abruptio placentae, bleeding from
vasa previa, ruptured uterus and heavy show.
· Non obstetric (local or incidental causes) include
1. PLACENTA PREVIA
1.1. Definition and grades
Placenta previa is bleeding from a placenta implanted in the lower uterine segment and thus
lies ahead of the presenting part.
· Grade 1 or low-lying placenta –the placenta occupies the lower uterine segment, but
does not reach the internal cervical os.
· Grade 2 or placenta previa marginalis—the placenta reaches the internal os but does
not cover it.
· Grade 3 or placenta previa partialis—the placenta covers the internal os but only
partially, even at full dilatation
· Grade 4 or placenta previa totalis--placenta covers the whole internal os even at full
cervical dilatation.
1.2. Incidence
1 in 200 to 250 deliveries it is more common in multiparas.
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72. Obstetrics and Gynecology
1.3. Predisposing factors
The exact cause is unknown, but there are a number of predisposing factors. These
include:
· Any uterine scar secondary to previous vigorous curettage, cesarean section,
myomectomy
· multiparity
· Bulky placental tissue as in multiple pregnancy and erythroblastosis fetalis
· Others include high altitude, smoking, previous history of antepartum hemorrhage.
1.4. Pathophysiology
Bleeding usually occurs in the third trimester when progressive formation of the lower
segment results in tearing and exposure of the blood vessels in the placental bed. The
bleeding is maternal in origin and is almost always revealed.
1.5. Clinical Features
The typical presentation is painless bright red bleeding in the third trimester which in
amount could range from spotting to massive. It tends to come without warning but may
follow coitus or pelvic examination. It is recurrent in nature with increasing bleeding
occurring in subsequent episodes.
Changes in maternal pulse, blood pressure and the degree of pallor are usually
proportional to the external blood loss. The usual findings on abdominal examination are
non-tender, normal-toned uterus (in labor relaxes completely between contractions); high
presenting part and abnormal fetal lie. Fetal distress occurs if the mother is in shock or in
labor as the result of downward pressure on the placenta.
Since it may be attended by severe bleeding, digital or speculum vaginal examination
should never be done in any woman with APH until placenta previa is ruled out.
1.6. Diagnosis
The diagnosis of placenta previa is strongly suggested by the clinical features discussed
above. Confirmation requires ultrasonographic localization of the placenta.
Ultrasonogrpahy is used to diagnose placenta previa and its grade as well as to evaluate
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73. Obstetrics and Gynecology
the condition of the fetus including its gestational age. Examination done before 30 weeks
should be repeated later as the position of the placenta may change as the lower segment
forms and increases in size.
Alternative method to diagnose placenta previa and its grade is to do vaginal examination
in the operating theatre with everything ready for caesarian section if necessary (double-set
up examination). This procedure can cause severe hemorrhage and thus should not be
routinely recommended. It should only be done in instances where ultrasound is not
available and termination of pregnancy is planned.
1.7. Management
All cases of suspected or proven placenta previa should be admitted and managed in a
hospital with 24 hours comprehensive emergency obstetric service including blood
transfusion. Early referral of patients from health centers to such facilities is crucial.
Women with life-threatening hemorrhage should receive aggressive resuscitation which
has to be started in the referring unit and continued during transportation. Patient should be
delivered by emergency caesarian section whatever the length of gestation or the grade of
the placenta previa is.
The management of women without severe bleeding requires admission to hospital.
Further management depends on the gestational age, condition of the fetus and extent of
bleeding. Termination of pregnancy either by induction (grade I and II anterior placenta
previa) or caesarian section (grade II posterior and IV placenta previa) should be done if
one of the following is present:
· Gestational age of more than 37 completed weeks
· Fetal death, fetal distress or presence of malformation incompatible with life
· Onset of active labor
· Continued bleeding after admission
In the absence of these conditions expectant management is followed. This includes
complete bed rest, avoidance of coitus or vaginal manipulation, and close clinical and
laboratory monitoring. Ferrous sulphate is routinely prescribed.
.
2. ABRUPTIO PLACENTA (ACCIDENTAL HEMORRHAGE)
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74. Obstetrics and Gynecology
2.1. Definition and classification
Abruptio placenta is premature separation of the normally implanted placenta before the
third stage of labor. The bleeding could be concealed (internal) or revealed (external) but in
most clinically apparent cases it is a combination of internal and external bleeding.
Depending on clinical and laboratory features, it is graded into mild (grade I), moderate
(grade II) and severe (grade III) types. Grades one and two each account for around 40%
while grade three only for 15%. The important features of the different grades are shown in
the table below.
Grade Bleeding Contractions BP HR FHR DIC
I Minimal complete
relaxation
Normal Normal Normal not present
II Mild-moderate
Incomplete
relaxation
Postural
hypotension
Increased distressed not present
III Moderate
to severe
Tetanic/
board like
Reduced/
unrecordable
Fast,
weak/
feeble
dead present
2.2. Incidence
It complicates 1% of all deliveries, the range being 0.3-1.6%.
2.3. Predisposing factors
The exact cause of abruptio placentae is unknown but there are a number of well-established
risk factors, including:
· Hypertensive disorders of pregnancy – single most important factor
· Trauma such as a hard abdominal blow
· Sudden decrease in uterine volume, as follows rupture of membranes in a mother
with polyhydramnios and following delivery of first twin
· Previous abruption placentae (recurrence is 10% after one episode and increases
to 25% after two)
· Others like poor socioeconomic condition and malnutrition, smoking and short
cord
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75. Obstetrics and Gynecology
2.4. Pathophysiology
An Abruptio placenta is typically an evolving process. The bleeding begins in arterial
vessels in the basal layer of the decidua, which is split by the hemorrhage. The retro
placental hematoma expands, compressing the placental tissue. This further separates the
placenta which in turn causes more bleeding and hematoma formation. Some of the retro
placental bleeding separates the membranes and escapes to the external. But most remain
concealed behind the placenta. With building pressure some of it splits the myometrial cells
causing bruised appearance of the uterus, the so called Couvelaires uterus. Occasionally
blood may find its way into the amniotic fluid resulting in bloody amniotic fluid. Damage to
the myometrium along with sequestration of clotting factors causes disseminated
intravascular coagulation. Profound shock eventually ends up in acute renal failure. Rarely
this process may be self-limiting.
2.5 Clinical Features and diagnosis
This varies with the grade of abruption. Vaginal bleeding, usually small in amount and dark
red in color is present in most. In some cases of concealed bleeding, this may be absent.
Abdominal pain of variable degree is another major manifestation, ranging from labor like
pain to unrelenting pain. In severe cases bleeding from the other site may occur. History of
hypertension, trauma and past history should be sought.
Vital signs derangement is indirectly proportional to the degree of blood loss. Abdomen is
almost always tender. In moderate cases there is incomplete relaxation between
contractions. In severe cases the uterus is board like and tetanically contracted uterus. The
fetus is in distress or dead. The presenting part is usually deeply engaged.
There are no specific diagnostic tests and therefore diagnosis is mainly made on clinical
grounds. Ultrasound is not helpful in diagnosis.
2.6. Complications
Common complications are severe bleeding and shock, consumptive coagulopathy, acute
renal failure, postpartum hemorrhage, fetal distress and intrauterine fetal death
2.7. Management
After admission one should secure an intravenous line, determine hemtocrite and blood
group / Rhesus factor assessment, prepare at least two units of cross matched blood.
Crystalloids should be administered depending on the needs. Assessment of the
coagulation factors using fibrinogen levels, prothrombin and partial thromboplastin times is
not feasible in most settings.
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76. Obstetrics and Gynecology
Simple bedside tests like whole blood clotting time and bleeding time can be used as rough
guides to the coagulation system. Fresh frozen plasma should be given in cases of
disseminated intravascular coagulation.
Unless there are contraindications, vaginal route of delivery preferred whether the fetus is
alive or dead. Labor is usually short and close fetal monitoring is needed to detect fetal
distress. Shortening of the second stage by instruments can be done. Unnecessary
episiotomy or laceration to the genital tract should be avoided. Third stage should be
managed actively.
Fetal distress in the first stage mandates caesarian section.
3. RUPTURE OF VASA PREVIA
Vasa previa develops when the fetal blood vessels course over the membranes and cross
the internal os in conditions such as placenta succenturiata and velamentous insertion of
the cord leading to bleeding from the fetal circulation.
It is a rare occurrence, the incidence being 1 in 5000 singletons, but much higher in
multiple pregnancies. Although a rare occurrence, it is yet very important because it leads
to fetal hemorrhage which frequently may result in fetal death and stillbirth.
This condition may be confused with placenta previa. The mother presents with painless
bright red bleeding which usually start after rupture of the membranes accompanied by
evidences of fetal distress.
Apt test is done to detect the presence of fetal blood in the vaginal blood. In this test few
drops of blood from the vagina is mixed with an equal amount of 25% sodium hydroxide.
Maternal blood will turn light brown, whereas fetal blood will not change color
because of its resistance to alkali.
A live viable fetus should be delivered immediately by emergency caesarian section as
even a small hemorrhage may be fatal. The neonatal hemoglobin should be determined
after birth.
4. OTHER CAUSES
Local lesions of the cervix and vagina such as vaginitis, cervicitis, cervical cancer or
polyps, foreign bodies, etc may cause vaginal bleeding in the antepartum period. Their
diagnosis depends on proper examination. Management depends on the cause.
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77. Obstetrics and Gynecology
Antepartum hemorrhage could originate from the placenta. Hemangioma of the placenta is
especially important. It occurs in approximately 1% of placentas. It sometimes may be
large enough to cause antepartum hemorrhage.
5. UNKNOWN CAUSES
These account for a significant proportion of cases of antepartum hemorrhage. In fact, in
many cases of antepartum hemorrhage, no cause is found. And some of these are thought
to be due to abruption placentae that are so small to be diagnosed by clinical evaluation or
special investigations.
GENERAL BASIC PRINCIPLES OF THE MANAGEMENT OF APH
I. Resuscitation should be started immediately, before referral if the later is contemplated.
II. All patients with APH should be admitted to a hospital.
III. No digital vaginal examination should be performed until a placenta previa has been
ruled out except under the condition of double-set up.
IV. Confirmation of the specific cause should be given emphasis in order to decide on the
specific management.
V. Mothers with antepartum hemorrhage, particularly abruption placentae, are at an
increased risk for postpartum hemorrhage. Thus universal active third stage management
has to be implemented.
Review Questions
1. Describe the major causes of antepartum hemorrhage and the clinical features that
may help to distinguish between them.
2. Describe the precautions that should be taken during evaluation and management of
a pregnant mother with antepartum hemorrhage.
CHAPTER 8
HYPERTENSIVE DISORDERS OF PREGNANCY (HDP)
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78. Obstetrics and Gynecology
Learning objectives
· To define hypertension and significant proteinuria during pregnancy
· To define pre-eclampsia and eclampsia
· To describe the features of severe pre-eclampsia
· To list the complications of pre-eclampsia
· To explain the basic principles of the management of eclampsia
· To identify the indications for termination of pregnancy in pre-eclampsia
Introduction
Hypertensive disorders (HDP) are one of the major causes of maternal death both in
developed and developing countries. They are also major contributors to intrauterine growth
restriction and intrauterine fetal death. Timely diagnosis and proper treatment can avert
these major complications and others.
1. Definitions:
Hypertension during pregnancy is defined as single blood pressure measurement of
160/110 mm Hg or more OR two consecutive blood pressure measurements of 140/90 mm
Hg or more measured on at least two occasions 6 hours or more apart.
Severe hypertension in pregnancy is defined as single measurement of diastolic blood
pressure of 120 mm Hg or more OR diastolic blood pressure 110 mm Hg or more on two
occasions measured 4 hours or more apart.
Significant Proteinuria in Pregnancy is defined as urinary protein excretion of 300 mg or
more per 24 hour (quantitative) OR 2+ or more protein on dipstick of two clean-catch
midstream specimens of urine collected 4 hours or more apart (qualitative).
Pathologic edema is defined as dependent edema that persists after nights rest OR any
type of non dependent edema that involves the face, the hands or the whole body OR
abnormal weight gain of more than 2 pounds per week.
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79. Obstetrics and Gynecology
Pre-eclampsia is occurrence of hypertension, proteinuria and/ or edema which occurs after
20 completed weeks of gestation and resolves within 6 weeks postpartum. Preeclampsia
before 20 weeks is associated with molar pregnancy. It is classified into mild and severe
forms. The presence of any of the following classifies it as severe preeclampsia.
· severe hypertension (refer definition)
· proteinuria of 5 grams or more in 24 hours (quantitative) or 3+ or more on dipstick on
two random specimens (qualitative)
· Oliguria (urine output of less than 400 milliliters in 24 hours) with or out raised renal
function tests.
· epigastric or right upper quadrant pain with or out elevated liver function tests
· Thrombocytopenia
· Cerebral symptoms like persistent frontal or occipital headache resistant to ordinary
analgesics, blurring of vision or scotoma, altered consciousness along with signs of
cerebral irritability like exaggerated deep tendon reflexes.
· intrauterine growth restriction
· pulmonary edema
· HEELP syndrome – haemolysis, elevated liver function test and thrombocytopenia
Chronic hypertension is hypertension that is present before pregnancy or is first detected
before 20 weeks of gestation and persists after 6 weeks postpartum with or without long term
complications.
Gestational or transient hypertension is recurrent mild hypertension that develops
between 20 weeks of gestation and 24 hours postpartum without other signs of preeclampsia
or chronic hypertension and resolves within 10 days postpartum.
Superimposed preeclampsia is worsening of hypertension (rise in systolic blood pressure
by 30 mmhg or/and rise in diastolic blood pressure by 15 mmhg from mid pregnancy levels)
and worsening or development of proteinuria with or without pathologic edema in a woman
with chronic hypertension.
Ecclampsia is tonic clonic convulsions or coma occurring during pregnancy, labour or within
7 days postpartum unrelated to other cerebral conditions like epilepsy in a woman with
neglected or fulminant preeclampsia. It occurs in 50 % antepartum, 25% intrapartum and
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80. Obstetrics and Gynecology
25% postpartum. Atypical ecclampsia is ecclampsia occurring before 20 weeks of gestation
and after 48 hours postpartum.
2. Incidence of HDP
Hypertensive disorders of pregnancy complicate 7-10% of pregnancies. Preecclampsia
occurs in 5% of pregnancies accounting for 70% of hypertensive disorders of pregnancy. The
incidence of ecclampsia is 0.1-0.5%.
3. Classification of HDP
Different classification schemes are used, some of which are complicated for routine use.
According to the American collage of Obstetricians and Gynecologists (ACOG) HDP is
classified into four.
· Preeclampsia ecclampsia syndrome
· Chronic hypertension
· Chronic hypertension with superimposed preeclampsia (pregnancy aggravated
hypertension)
· Gestational or transient hypertension
In some cases it becomes difficult to classify hypertension into any of the groups because of
inadequate information like unknown gestational age, hypertension that is first detected after
20 weeks, labour or postpartum period. In these cases it is best to manage them as having
preeclampsia.
Some use the term pregnancy induced hypertension (PIH) to describe
preeclampsia/ecclampsia and gestational hypertension.
4. Etiology of pre-eclampsia
The exact cause of pre-eclampsia is unknown. A number of theories are forwarded, so
preeclampsia is said to be a disease of theories.
5. Risk factors for preeclampsia
Risk factors associated with pure preeclampsia are
· nulliparity especially at extremes of reproductive age (less than 20 and greater
than 35 years)
· conditions with hyperplacentosis (multiple pregnancy, RH isoimmunization, non
immune hydrops fetalis)
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81. Obstetrics and Gynecology
· molar pregnancy
· family history of pre-eclampsia in mother or sister
· new paternity
· black race and low socioeconomic status
Risk factors associated with superimposed preeclampsia are
· chronic hypertension before pregnancy
· strong family history of hypertension
· chronic renal disease
· diabetes mellitus
· connective tissue disorders
6. Pathophysiology of pre-eclampsia and eclampsia
The hallmark in the pathophysiology of preeclampsia is widespread vasoconstriction which
results in marked increase in peripheral resistance. This process starts 3-4 months prior to
the development of hypertension. The subsequent effects of this change are:
· Development of arterial hypertension which is proportional to the increase in
peripheral resistance. In severe cases decrease in venous return may lead to
normotensive preeclampsia.
· Decreased blood volume from reduced vascular space. Preeclamptic women,
therefore, can not tolerate blood loss at any time during pregnancy and delivery.
· Decreased tissue perfusion resulting in capillary endothelial damage in various
organs. In the kidneys it is called glomeruloendotheliosis and manifests with
proteinuria (albuminuria).
· Increased capillary permeability results in increase in interstitial fluid resulting in
edema formation and concomitant reduction in intravascular volume which results in
hemoconcentration.
· Capillary endothelial damage results in the formation of micro thrombi in different
organs mainly liver, kidneys, brain. This results in reduction in platelet count and
other clotting factors.
7. Complications of preeclampsia
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82. Obstetrics and Gynecology
Preeclampsia, if untreated, is associated with high maternal and perinatal mortality and
morbidity. The common complications are eclampsia, abruptio placenta, acute renal
failure, hepatic failure and rupture of subcapsular hematoma, HEELP syndrome and
disseminated intravascular coagulation, cerebral hemorrhage and pulmonary edema and
heart failure. Intrauterine growth restriction and death are fetal complications.
8. Diagnosis and clinical evaluation
The diagnosis of hypertensive disorders of pregnancy is straight forward. The major task
is to differentiate between different types of HDP (mild and severe preeclampsia, chronic
hypertension, superimposed preeclampsia) and identify presence of complications. To
achieve this complete history, physical examination and necessary investigations should
be carried out.
Important points that should be included in the history are:
· Gravidity, parity, gestational age and marital history for new paternity
· Symptoms related to pathologic edema: leg swelling that persists after rest, tightness
of the rings, puffiness of the face,
· Symptoms related to severe preeclampsia: decrease in urine output, fetal movement,
· Symptoms of imminent eclampsia: severe and persistent global or occipital
headache, blurring of vision, epigastric or right upper quadrant pain
· Presence of convulsions
· Symptoms of long term complications of chronic hypertension: visual symptoms,
neurologic symptoms, cardiac symptoms
· Past or family history of hypertension and drugs used in treatment
· History of renal disease and other medical illnesses
· Treatment received so far
Important areas to emphasize in the physical examination are:
· Blood pressure and weight
· Fundal height and fetal heart beat
· Dependant and non dependent edema: pitting pedal and pretibial edema, abdominal
wall edema, periorbital edema, ascitis
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· Cardiac vascular examination: cardiomegally, murmurs, peripheral pulses and renal
artery bruit
· Deep tendon reflexes, fundoscopy, sensory and motor functions
Depending on the availability the laboratory investigations include:
· Urine protein: mid stream urine for dipstick (more applicable) and 24 hour urine
protein
· Complete blood count: hemtocrite, platelet count
· Blood chemistry: renal and liver function tests, uric acid
· Ultrasonography : gestational age, biophysical profile
9. Management
I. Preeclampsia
Termination of pregnancy is the definitive and curative treatment for preeclampsia resulting
in resolution of the condition within 48 hours. It is the most appropriate treatment for the
mother. Any management short of this is palliative and should have the objective of reducing
the perinatal mortality associated with preterm birth.
The factors that determine whether to embark on aggressive (delivery) or conservative
management are the gestational age, the severity of the disease, the fetal maturity and fetal
condition.
A. Aggressive management
Indications for aggressive management are gestational age of 37 weeks or more, mature
fetus as evidenced by lung maturity tests, severe preeclampsia, worsening preeclampsia
despite conservative management, imminent ecclampsia, ecclampsia, HEELP syndrome and
fetal compromise (fetal distress, abnormal fetal wellbeing tests or fetal growth restriction).
Important components are
Administer short acting antihypertensive drugs like hydralazine (5 mg IV stat followed by 5
mg in 10 minutes, then 5-10 mg every 20 minutes to a maximum of 60 mg)or nifedipine(10
mg sublingual to be repeated after 30 minutes) intermittently when the diastolic blood
pressure is 110mmhg or more. Excessive lowering of the blood pressure compromises
placental perfusion and should be avoided.
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Start infusion of parenteral anticonvulsants using diazepam (10-20 mg by slow IV bolus over
2-3 minutes followed by slow IV infusion of 30-40 mg in 1000 ml of 5% dextrose in water over
24 hours. 10 mg IV bolus can be repeated if convulsions recur) or magnesium sulphate
Depending on the prevailing conditions, decide on the mode of delivery (either by induction
or caesarian section). Since these women are anesthetic risks, caesarian section is reserved
for those with contraindication for induction. (Refer to chapters 15 and 16).
Monitor frequently blood pressure, deep tendon reflexes, urine output, level of consciousness
and if being induced monitor induction according to the protocol hourly,
For vaginal delivery, shorten the second stage by instrumental delivery
In the third stage, do not give ergometrine
Continue monitoring the blood pressure, the level of consciousness, the deep tendon
reflexes, the urine out put
Continue antihypertensive. Continue anticonvulsant infusion for at least 24- 48 hours
postpartum.
B. Conservative management
Based on the above considerations, if termination is not indicated and the decision is to
postpone delivery, then
Admit all cases to a hospital setting capable of managing complications
Perform base line history, physical examination and investigations as described in subtopic
8.
Order bed rest in left lateral position, with necessary mobility permissions. Do not restrict salt
intake. Restrict visitors.
Take daily history of headache, blurring of vision, right upper quadrant pain, urine output,
fetal movement (kick chart), extent of edema
Measure blood pressure frequently (every 15 minutes to every 6 hours, depending on
severity)
Record weight, edema, deep tendon reflexes, fetal heart beat and urine out put daily,
Monitor fetal growth by fundal height or ultrasound weekly
Monitor fetal well being two or more times a week
Monitor urine albumin daily
Monitor uric acid, renal and liver function tests, platelet and hemtocrite weekly
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Start medium acting antihypertensive like alpha methyl dopa (250-500 mg 6-hourly) only if
the diastolic blood pressure is 100mmhg or above. Diuretics and angiotensin converting
enzyme inhibitors are contraindicated.
Once the condition of the patient is stabilized, she may be discharged and followed as an
outpatient provided that blood pressures is between 140-160/90-100 mm hg, proteinuria is
1+ or less by dipstick or less than 500 mg in 24 hrs, there is no fetal jeopardy and the patient
is compliant.
Outpatient management consists of frequent ANC follow up with blood pressure and
random urine protein measurements at least twice per week and daily fetal movement
counting by the mother. The mother should be educated about the imminent
symptoms and signs and warned of the need to report immediately if she has any of
them at any time.
II. Eclampsia
This is an acute obstetric emergency which if not managed appropriately results in the
death of the mother and the fetus.
Start the ABC of resuscitation (clear the airway by suction, start an intravenous line, position
the woman in lateral position to prevent aspiration, administer oxygen nasally and if in
respiratory arrest assist ventilation artificially)
Prevent trauma to the tongue by inserting a mouth gag and fall accidents by bed rails
Catheterize the bladder by an indwelling folley catheter
Order necessary investigations
Start short acting antihypertensive as described above
Start anticonvulsants as described in aggressive management
Terminate the pregnancy as described in aggressive management. Unfavorable cervix is
usually an indication for caesarian section.
Monitor the patient as described in aggressive management but more aggressively (vital
signs including respiratory rate, pulse rate and temperature every half to 1 hour)
Continue monitoring for 24 -48 hours after delivery. If the patient convulses later than 48
hours after delivery, other possible causes should be entertained.
Review Questions:
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1. Define the following: Hypertension during pregnancy: Significant proteinuria during
pregnancy and Pre-eclampsia and eclampsia
2. List the risk factors and complications of pre-eclampsia.
3. List the features of severe pre-eclampsia
4. Outline the management of pre-eclampsia and eclampsia
CHAPTER 9
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DISTURBANCES OF AMNIOTIC FLUID VOLUME
Learning Objectives
· To discuss the mechanism of production and absorption of amniotic fluid
· To list the important functions of amniotic fluid
· To list the causes and complications of polyhydramnios
· To list the causes and complications of polyhydramnios
1. INTRODUCTION
Amniotic fluid invests and protects the fetus during its intrauterine life, growth and
development. Its volume has an average value in normal pregnancy but there may be
abnormalities of this volume (excess or reduction) which indicate the presence of an
underlying problem in the fetus and which also may result in certain complications.
Abnormally small volume of amniotic fluid is especially more associated with serious
problems in the fetus compared to excess.
1.1. Production and Absorption of the amniotic fluid
In the first trimester amniotic fluid is produced as the feto-maternal serum dialysate or ultra
filtrate. In the second and third trimester its source is mainly fetal urination. Secretions by the
pulmonary epithelium and amnion cells also have some contributions.
Fetal swallowing is the major mode of absorption of amniotic fluid. Some is absorbed by the
pulmonary epithelium.
The normal volume at term is 500 to 1200 ml, the average being 800 ml.
1.2. Functions of amniotic fluid
· It acts as a cushion against trauma
· It also acts as a constant temperature buffer
· It functions as a waste deposit area
· It plays important role in the development of the renal, gastrointestinal and
pulmonary systems and the development of fetal musculature
· It forms a reservoir for proteins, minerals and fluid.
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· It prevents the skin and eye from drying.
2. POLYHYDRAMNIOS (HYDRAMNIOS)
2.1. Definition
Polyhydramnios refers to term amniotic fluid volume of more than 2000 ml. But this is usually
not practical and the diagnosis is based on clinical evaluation and ultrasound assessment of
the volume of the amniotic fluid. At term amniotic fluid pool of more than or equal to 8
centimeters and /or an amniotic fluid index (AFI) of more than or equal to 20-25 cm are
suggestive.
Hydramnios may be acute or chronic. The acute form tends to develop rapidly in the third
trimester and usually causes greater discomfort to the mother.
2. 2. Etiology
Majority of polyhydramios is idiopathic (>60 %). The rest arise either from conditions that
increase the surface area of the placenta and amnion or disrupt the integument of the fetus
or hamper the normal swallowing process of the fetus. Diabetes mellitus, placental tumors,
fetal anomalies like esophageal atresia, tracheoesophageal fistula, spina bifida and
anencephaly, RH isoimmunization, nonimmune hydrops and multiple gestations are clinical
conditions associated with polyhydraminos
2.3. Clinical Features and diagnosis
Symptoms are purely mechanical, arising from pressure within or around the distended
uterus. Abdominopelvic discomfort, shortness of breath, edema of the lower limbs and lower
abdomen and in severe cases decreased urine output could be reported by the patient.
These could be exaggerated in acute cases.
The finding of big-for-date uterus, difficulty to feel fetal parts, easy ballotment of the fetus and
distant or faded fetal heart tones should arouse suspicion.
Ultrasound is the method of confirming the diagnosis.
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2.4. Complications
Premature rupture of the membranes, preterm labor, malposition and malpresentation,
abruption placentae and postpartum hemorrhage should be anticipated. Increased rate of
operative deliveries also occurs.
2.5. Management
Management is best done in well equipped settings capable of handling the complications.
Termination of pregnancy is the management of choice for polyhydramnios caused by
malformations incompatible with life. In the absence of this termination should be delayed as
much as possible until fetal maturity. Bed rest along with serial therapeutic amniocentesis is
the modalities of treatment. Non steroidal anti-inflammatory drugs like indomethacin can be
given.
3. OLIGOHYDRAMNIOS
3.1. Definition
Oligohydramnios is term used when amniotic fluid volume of less than 500 milliliters. The
ultrasound criterion for diagnosis is amniotic fluid pool of less than 1-2 centimeters and/or an
AFI of less than 5-7 centimeters.
3.2. Etiology
Prolonged rupture of membranes is the most common cause. Others are postdate
pregnancy, intrauterine growth retardation or death, congenital anomalies especially renal
agenesis and drugs such as angiotensin converting enzyme inhibitors.
3.3. Clinical Features
Symptoms, if present, reflect the underlying condition. The common sign is small-for-date
uterus.
3.4. Complications
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Pulmonary hypoplasia, cord compression and amniotic band syndrome are known
complications of prolonged oligohydramnios. Intrauterine fetal death and variable
decelerations in labor are others.
3.5. Management
Treatment is directed against the cause. Immediate delivery is the best management for an
alive fetus nearing maturity. Continuous intrapartum monitoring is needed to detect
deceleration from cord compression. Aminioinfusion, where practiced, can be used in
pregnancies remote from term. Termination of pregnancy should be considered if congenital
malformation is the cause.
Review Questions
1. Discuss the production and absorption of amniotic fluid.
2. Describe the clinical features and complications of polyhydramnios.
3. Describe the complications of oligohydramnios.
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CHAPTER 10
PREMATURE RUPTURE OF MEMBRANES (PROM)
AND PRETERM LABOR
Learning Objectives
· To define premature rupture of membranes and preterm labor
· To list the risk factors for premature rupture of membranes
· To list the risk factors for preterm labor
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92. Obstetrics and Gynecology
· To describe the diagnosis of PROM
· To list the complications of premature rupture of membranes
· To outline the management of PROM
· To discuss the contraindications for suppression of labor in a mother with
premature labor
1. PREMATURE RUPTURE OF MEMBRANES (PROM)
1.1. Definition
Premature rupture of membranes is rupture of membranes at least one hour before the
onset of labor, regardless of the gestational age. It is further subdivided into preterm PROM
and term PROM depending on whether the rupture of membranes occurred before or after
37 completed weeks of gestation.
Latency period is defined as the period between the time of rupture of membranes and the
onset of true labor. If the latency period extends more than 24 hours it is called prolonged
premature rupture of membranes.
1.2. Incidence
It varies widely ranging between 6-12%. Majority occur at term.
1.3. Etiology
In most no apparent cause is found, but a number of conditions that either increase
intrauterine pressure or reduce the strength of the membranes are implicated.
Chorioamnionitis, polyhydramnios, multiple pregnancies, cervical incompetence, trauma and
a variety of lower genital tract infection are clinical conditions that in one way or another
associated with PROM.
1.4. Clinical features and diagnosis
History gives unequivocal diagnosis in most cases. In typical cases the patient gives history
of sudden gush of clear fluid per vagina followed by persistent uncontrolled leakage. In less
typical cases one may get small intermittent leakage of clear fluid.
Physical examination in typical cases will reveal moist perineum with amniotic fluid seen
flowing from the vagina. Digital pelvic examination should not be done in a patient suspected
of having PROM unless delivery is planned in 24 hours. Instead, sterile speculum
examination is done to confirm the diagnosis.
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93. Obstetrics and Gynecology
During the speculum examination, finding a pool of amniotic fluid in the posterior fornix and
observing amniotic fluid trickling from the cervical opening clinches the diagnosis. Performing
Valselva maneuver of application of fundal pressure may help.
If in doubt, additional tests can be done to confirm the diagnosis. These include tests that
rely on amniotic fluid characteristics. Nitrazine paper test (changes from yellow to deep blue)
and litmus test (changes from red to blue) is based on the alkaline nature of the amniotic
fluid. Ferning test (air drying a drop of the fluid on a slide and examine for arborization under
light microscopy) is positive.
Other tests like dye instillation tests are not routinely done. Ultrasound is not helpful but may
give indirect evidence if one finds oligohydramnios.
1.5. Complications
PROM is associated with increased maternal and perinatal morbidity and mortality.
Intrauterine infection (chorioamnionitis)
Umbilical cord prolapse and compression
Malpresentation
Preterm labour and its complications
Oligohydramnios, if prolonged causes pulmonary hypoplasia and compression deformities
Abruptio placenta
Neonatal complications mainly congenital pneumonia and sepsis and the effects of
prematurity
1.6. Management
The management depends on the presence or absence of chorioamnionitis, fetal distress or
death or established labour. In the absence of these management depends on the
gestational age.
I. Complicated PROM
Delivery should be accomplished in the presence of the following. Depending on the existing
conditions, the route of delivery can either be vaginal or abdominal.
A. Chorioamnionitis
Diagnostic features are fever with chills, abdominal pain, offensive amniotic fluid,
tachycardia, uterine tenderness and fetal tachycardia. Leukocytosis with left shift is often
found. Diagnosis is confirmed by finding microorganisms in amniotic fluid sample.
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94. Obstetrics and Gynecology
The complications are sepsis, septic shock and neonatal sepsis.
Management is administration of broad spectrum antibiotics (ampicillin and gentamycin) and
termination of pregnancy preferably by induction. Antibiotics should be continued after
delivery. The neonate should be treated by combination ampicillin gentamycin
intramuscularly.
B. Fetal distress
C. Fetal death
D. Established labour
II. Uncomplicated PROM
Management depends on the gestational age.
A. Gestational age of 34 weeks or more
The risk of intrauterine infection is higher than the risk of prematurity. Therefore, delivery of
the fetus by induction or caesarian section should be done. Some wait for 12-24 hours in
hope of spontaneous onset of labour.
B. Gestational age of less than 34 weeks
The risk of prematurity is higher than the risk of intrauterine infection. Therefore,
postponement of delivery till fetal maturity (or 34 weeks) while closely monitoring for
complications is the management of choice.
Admit the woman.
Monitor the vital signs every 6 hours.
Monitor for uterine contraction, uterine tenderness and fetal well being (fetal heart beat and
kick chart) on daily basis (or more frequently).
Monitor the white cell count daily.
Monitor fetal growth by fundal height or by ultrasound every week. Check for lung maturity
Prophylactic antibiotics and tocolytics are not generally advised.
2. PRETERM LABOR
2.1. Definition
Preterm labor is the onset of regular uterine contractions and progressive cervical
dilatation and effacement occurring between 28 and 37 completed weeks of gestation
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95. Obstetrics and Gynecology
resulting in the birth of a physically immature neonate with birth weight between 1000 and
2499 grams.
It is classified as spontaneous and induced preterm labour.
2.2. Incidence and importance
Preterm labour complicates 5-15% of all deliveries. Its importance lies on its effect on the
perinatal outcome. It accounts for up to 80% of neonatal deaths in some institutions. Mortality
is mainly related to gestational age at birth. Four of the six major causes of neonatal deaths
are associated with preterm labour. Survivors have increased risk of cerebral palsy and
mental retardation. The cost of caring the preterm neonate is very high.
2.3. Etiology and risk factors of spontaneous preterm labour
The exact cause is unknown. Risk factors are identified in only 50 % of the cases. These risk
factors are
Past obstetric and gynecologic factors: uterine anomaly (like unicornuate and bicornuate
uterus), submucosal myomas, cervical incompetence, previous preterm labour
Current pregnancy complications: PROM, polyhydramnios, multiple gestation, amniotic fluid
infection syndrome,
Surgical/ medical complications: acute febrile illnesses, abdominal surgery especially on
appendix and adenexa, penetrating abdominal trauma, asymptomatic bacteruria
Demographic factors: non white race, low socioeconomic status, maternal age of lees than
18 and greater than 40, smoking, alcohol abuse, exhausting work
2.4. Diagnosis
Diagnosis is based on the following findings
· Gestational age between 28 and 3 completed weeks plus
· Regular uterine contractions occurring 5- 8 minutes apart or closer (others use 4
contractions in 20 minutes or 8 in 60 minutes) each with duration of more than 30
seconds plus
· Any one of the following with or without ruptured membranes ( cervical effacement of
more than 80 or dilatation of the cervix of 3 cms and more or progressive change in
the cervix over time by digital examination or ultrasound)
2.5. Prevention
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A variety of regimens have been used to reduce the occurrence of spontaneous preterm
labour in those with risk factors but all with limited success. These include
Intensive patient education programs with weekly pelvic examination or serial ultrasound
Limiting activity to bed rest in late second and early third trimester
Adequate hydration
Treating treatable medical conditions like febrile illnesses, asymptomatic bacteruria and
vaginal infections
Others like prophylactic tocolysis and cerclage
In induced preterm labour iatrogenic immaturity should be prevented as much as possible.
This is done by ensuring the gestational age and performing fetal lung maturity test.
2.6. Management:
Labour is allowed to continue in the following conditions. Preparations must be made to
manage/prevent complications in the newborn.
Fetal: fetal death, major malformation, fetal distress, multiple gestation, intrauterine growth
restriction, gestational age of more than 34 weeks
Maternal: APH, severe preeclampsia, cardiac disease and others
Others: PROM, chorioamnionitis, advanced labour (cervix greater than 3 cm)
In the absence of the above factors conservative management can be instituted. For the
interest of the newborn such management should be given in a setting with intensive
neonatal care unit (referral to such setting is essential). These include
Non specific measures with bed rest, rapid hydration and sedation
In the absence of contraindications, suppression of labour by using B mimetic drugs (like
ritodrine or terbutaline) or magnesium sulphate
Acceleration of fetal lung maturity by corticosteroids like betamethasone or dexamethasone
given at least 24 hours before delivery.
2.7. Intrapartum Management]
This is generally similar to the management of labor at term except that certain precautions
are necessary in order to prevent complication in the neonate. Among these is the prevention
of intracranial hemorrhage during labor. Intraventricular hemorrhage affects 30-60% of all
very low birth weight babies, the majority of whom are preterm. Measures that can be taken
to minimize this risk are:
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97. Obstetrics and Gynecology
Prevention of intrapartum hypoxia
Perform controlled delivery of the fetus. Forceps delivery is usually recommended for the
same reason as an episiotomy; but it may prove harmful in some cases
Elective cesarean section is a preterm baby is growth-retarded and also with a breech
between 1000 and 1500 grams
2. 7. Neonatal complications
Respiratory distress syndrome (hyaline membrane disease), intraventricular hemorrhage,
hypothermia, hypoglycemia, cerebral palsy, congenital malformations and mental retardation
are some of the major complications that contribute to mortality and morbidity of theses
newborns.
For these reasons all preterm neonates require close medical care after delivery.
2.8. Contraindications for suppression of labor
· Fetal: intrauterine fetal death, congenital abnormalities incompatible with life,
pregnancy of gestational age more than 34 weeks or proven lung maturity, fetal
distress, intrauterine growth restriction, PROM, multiple gesation
· Maternal: intrauterine infection (chorioamnionitis),complications that necessitate
delivery like severe preeclampsia, APH,
· Conditions that contraindicate the administration of tocolytics like cardiac diseases,
uncontrolled diabetes, thyrotoxicosis
Review Questions
1. Define premature rupture of membranes and preterm labor
2. Describe the diagnoses of premature rupture of membranes and preterm labor.
3. List the complications of premature rupture of membranes.
4. Describe the risk factors for preterm labour.
5. Discuss the management of premature rupture of membranes.
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CHAPTER 11
MULTIPLE PREGNANCY
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Learning Objectives
· To discuss the different types of multiple pregnancy
· To describe the risk factors for multiple pregnancy
· To list the maternal and perinatal complications of multiple pregnancy
· To discuss the clinical features and the diagnosis of twin pregnancy
· To describe the antepartum, intrapartum and postpartum management of twin
pregnancy
1. Introduction
Multiple pregnancy (also called multiple gestation) is a pregnancy with more than one fetus.
It is a high-risk pregnancy associated with significantly higher rates of maternal and perinatal
morbidity and mortality. Therefore, mothers with multiple pregnancy will need special
antepartum, intrapartum and postpartum care which ideally should be provided in specialized
centers (at least in a hospital).
Multiple pregnancies include twins, triplets, and quadruplets and higher order pregnancies,
but the most common of these is twin pregnancy and the following discussion will focus on
twin pregnancy.
2. Types and incidence of twin pregnancy
Depending on the number of ova involved, twin pregnancy is divided into two types.
Dizygotic twins (fraternal twins) result from fertilization of two separate ova by two
spermatozoa. They are always diamniotic – dichorionic and usually have separate placenta.
Their sex may or may not be the same. Their genetic content is different.
It accounts for two-thirds of twin pregnancy. The incidence varies, ranging between 1.3 and
49 per 1000 pregnancies. A traditional method of approximation (Hellin’s rule) is used to
estimate the incidence of multiples roughly:
Incidence=1:80n-1 where n is the number of fetuses.
There are several factors that increase the incidence of dizygotic twins. These are
Race (more in blacks than whites)
Family history of twinning especially on the maternal side
Increasing maternal age (the peak maternal age for dizygotic twinning is 35-40years)
Previous history of twin pregnancy
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100. Obstetrics and Gynecology
Pregnancy soon after stopping oral contraceptives (greater rebound gonadotrophin
secretion)
Ovulation induction using human pituitary gonadotrophins or clomiphene citrate (this may
also increase the incidence of monozygotic twinning) and
Assisted reproductive technology.
Monozygotic twins (identical twins) result from division of a single zygote. They have
identical genetic material and are always of same sex. They have one placenta but other
features depend on the time of division of the fertilized ova.
If division occurs before 72 hours of fertilization a diamniotic-dichorionic placenta with
two fetuses result accounting for 30% of monozygotic twins.
If division occurs between the third and eights day of fertilization, a diamniotic-monochorionic
placenta with two fetuses result which makes up 69% monozygotic twins.
If division occurs between eight and thirteen days a monoamniotic-monochorionic
placenta with two fetuses result making up <1% of monozygotic twins.
If division occurs after day 13 conjoined twins/ Siamese twins result. These could be
pygopagus (sacro-coccyx), thoracopagus (thoracic cage), omphalopagus (area between the
umbilicus and the xiphysternum), thoraco-omphalopagus (a combination of the above two)
and craniopagus (cranium).
Further postponement of division after day 16 results in incomplete twinning producing, for
example, twins with two heads but a single body (dicephalus).
Monozygotic twins account for around a third of twins. The incidence is random and constant
throughout, ranging between 2.3 and 4 per 1000 pregnancies. Unlike dizygotic twins, there
are no known risk factors.
3. Determination of zygocity
Following delivery one can determine the zygocity in the following manner. First look at the
sex of the twins. If they are different then the zygocity is dizygotic. If the sex is the same
proceed further to examine the placenta and the membranes. Presence of only one placenta
without dividing membranes or dividing membrane with only two layers confirms monozygotic
twins. Presence of one placenta with four layered dividing membrane or presence of two
placentas can exist in both monozygotic and dizygotic twins. For these cases further
evaluation is needed like determining the blood group of the neonates or DNA fingerprinting.
Antenatal determination of zygocity is possible by ultrasonography.
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4. Diagnosis
Early diagnosis is important for successful outcome. The diagnosis of multiple pregnancy
needs a high degree of suspicion.
Suggestive symptoms are exaggerated pregnancy symptoms like excessive vomiting,
abnormally fast increase in abdominal girth and excessive fetal movement. Risk factors like
family and personal history of twinning may be present.
Physical findings include large-for-date uterus, feeling of multiple fetal parts with three poles
identified and auscultation of two or more distinctly different fetal heart beats with difference
of at least 10 beats/ minute. Abnormal increase in weight, anemia and preeclampsia are
common.
Confirmation of the diagnosis needs performing ultrasound or plain abdominal X-ray.
Ultrasound is the best method because besides confirming the diagnosis it also checks for
the gestational age, malformation, placental localization and zygocity.
5. Complications
Generally perinatal morbidity and mortality is increased in multiple pregnancy as compared
to singletons. This is more so with monozygotic twins especially if they are of monoamniotic
type. The second twin is usually the smaller and will suffer more from the effects of abruption
placentae, hypoxia, constriction ring dystocia, operative manipulation and prolonged
anesthesia. Maternal morbidity is also increased by 3- 7 times.
Multiple pregnancy is associated with almost all known complications of pregnancy, childbirth
and postpartum period.
Antepartum complications include spontaneous abortion, congenital malformations,
hyperemesis gravidarum, preeclampsia/ ecclampsia, antepartum hemorrhage, PROM and
preterm labor, intrauterine growth restriction, malpresentations, polyhydramnios, anemia and
cord accidents (compression, entanglement and prolapse).
Intrapartum complications include uterine dysfunction, malpresentation in labour (40% are
vertex-vertex, 35% are vertex-breech or vise versa, 10% are breech-breech, 10% are
transverse with breech or vertex and rarely both may be transverse), increased operative
delivery especially caesarian section, cord prolapse and retained second twin.
Postpartum complications include postpartum hemorrhage and puerperal sepsis.
Complications unique to multiple pregnancy include discordant twins, intrauterine fetal
death of one twin, twin to twin transfusion and conjoined twins.
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6. Differential diagnosis of big for date uterus
These are wrong date, macrosomic fetus, polyhydramnios, molar gestation, abdominal tumor
with the pregnancy such as fibroids or ovarian masses and in early pregnancy full bladder.
7. Management
7.1. Ante partum management
Since multiple pregnancy is a high-risk pregnancy requiring specialized care, diagnosing the
pregnancy as early as possible is essential. These mothers are followed as high-risk with
more frequent antenatal visits. Tasks to be performed during the antenatal period are
· Dietary advice on the need to take more calories, proteins and vitamins
· Supplementation with iron and folic acid
· Frequent and careful fetal monitoring using fundal height, kick chart and where
available serial ultrasound and fetal wellbeing tests
· Provision of adequate rest especially after the 24th week
· Prevention, if possible, and/or early detection and treatment of complications
(including referrals) associated with multiple pregnancies.
· Education on the need for hospital delivery
· Decision on the mode of delivery, which in the absence of other complications, is
determined by the number of fetuses, the presentation of the first twin and the
presence of conjoining. Caesarian section is indicated in triplets and above, if the first
twin is non vertex and in conjoined twin.
7.2. Intrapartum management
Ideally, labour should be attended in a hospital setting with personnel skilled in intrauterine
manipulation and neonatal resuscitation and with capacity to monitor both fetuses and with
set up to perform emergency caesarian section and blood transfusion and with set up for
intensive neonatal care. At least delivery should be in a hospital with facilities for caesarian
section.
In the first stage, admit the patient in early labor, secure an intravenous line and start
infusion of crystalloids. A minimum of two units of blood should be cross matched. Close
monitoring of the vital signs, uterine contractions and fetal heart beat of both fetuses should
be done. Monitor progress of labour by periodic cervical examination. If labour is prolonged
caesarian section must be done. Augmentation is contraindicated.
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In the second stage, deliver the first twin. Clamp and cut the cord. Immediately following this
perform abdominal palpation to determine the lie of the second twin and auscultate for its
fetal heart beat. Assess also the degree of vaginal bleeding.
Await spontaneous delivery if the lie is longitudinal and there is no fetal distress or excessive
vaginal bleeding. Augment with oxytocin If uterine contractions are not adequate.
If the lie is transverse one should attempt external cephalic version. If successful proceed as
above. If this fails either perform internal podalic version followed by total breech extraction.
This should only be done by persons with considerable expertise in an operating theatre. If
this can not be done the second twin should be delivered by caesarian section.
In the presence of fetal distress or excessive vaginal bleeding deliver the second twin fast by
instrumental delivery (if vertex) or by total breech extraction (if breech) or by internal podalic
version and breech extraction (if transverse) or by caesarian section (if the above procedures
are contraindicated or have failed).
Third stage is managed actively. The placenta and the membranes are delivered with care
for subsequent examination.
Review Questions
1. Describe the two types of twin pregnancy.
2. List the factors that increase the risk of dizygotic twinning.
3. List the complications of multiple gestation in the antenatal period.
4. Discuss the diagnosis of multiple gestation.
5. Outline the intrapartum management of twin pregnancy.
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CHAPTER 12
RH ISOIMMUNIZATION
Learning Objectives
· To define Rh isoimmunization and hemolytic disease of the newborn
· To describe the pathogenesis of Rh isoimmunization
· To describe the effects of Rh isoimmunization on the fetus-newborn
· To outline the management of Rh negative unsensitized pregnancy.
1. Introduction
Many different antigens are found on the surfaces of red blood cells and they may cause
important isoimmunization in obstetrics. The most important of these is the Rh group.
Next to the ABO system, the Rh system is the second most important blood group system.
The Rh antigens are found on red blood cell membrane protein. Although more than 40
different antigens in the Rh system have been described, five determinants account for the
vast majority of phenotypes. One of the systems used to designate Rh antigens is the
Fishers CDE system. Inheritance of Rh antigens follows Mendellian law, which is an
individual is either homozygous or heterozygous for each antigen.
The D antigen, also called the Rh factor is the most powerful and important of the Rh
antigens. An individual who possess it is labeled as Rh positive and who lack it as Rh
negative. Some people react weakly to anti D antibody and are labeled as Du positive. The
incidence of Rh negative people varies from population to population (15% in Caucasians
and 4% in African blacks). Exposure of these Rh-negative people to even small amounts of
Rh-positive cells, by either transfusion or pregnancy, can result in the production of anti-D
alloantibody, a condition called Rh sensitization or isoimmunization.
2. Definitions
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I. Rh incompatibility is the presence of different Rh types in a woman and her partner. In
obstetrics, the significant incompatibility is when the woman is Rh negative and the partner is
Rh positive.
II. Rh isoimmunization (Rh sensitization) is production of antibody against the Rh factor by
an Rh negative woman following exposure to Rh-positive cells.
III. Erythroblastosis fetalis is the condition in which large numbers of nucleated red cells
are seen in the fetal circulation, occurring in response to excessive destruction of fetal red
blood cells.
.IV. Hydrops fetalis is generalized edema in the fetus and collection of serous fluid in body
cavities of the fetus resulting from a variety of pathologic conditions (immune hydrops and
non immune hydrops).
V. Hemolytic disease of the newborn is occurrence of progressive anemia and
hyperbilirubinemia in a newborn caused by haemolysis of red blood cells, in most cases
antibody mediated.
3. Pathogenesis
For Rh isoimmunization to occur, the following prerequisites must be fulfilled:
I. Rh negative mother carrying Rh positive fetus
The chance of having Rh positive fetus from Rh positive father ranges from 50% (if the father
is heterozygous) to 100% (if the father is homozygous). Non paternity explains the
development of hemolytic disease of the newborn.
II. Entry of the fetal Rh positive red blood cells into maternal circulation
This occurs following transfusion of incompatible blood (rare nowadays because of screening
before transfusion) or more commonly following fetomaternal hemorrhage (through leaks in
the placenta).
Fetal red blood cells are detected in maternal circulation in 6% in the first trimester, 15% in
the second trimester and 30% in the third trimester. It may be silent or may follow obstetric
complication. Fetomaternal hemorrhage occurs in more than 50% during delivery especially
in the third stage. Conditions that aggravate fetomaternal hemorrhage are spontaneous or
induced abortion, ectopic gestation, antepartum hemorrhage especially abruptio placenta,
amniocentesis, abdominal trauma, and external cephalic version. Conditions that worsen
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fetomaternal bleeding during labour are manual removal of placenta, twin delivery and
caesarian section.
III. Development of Rh antibodies by the mother
The maternal immune system responds by producing antibodies which are initially of Igm
type (big immunoglobulin that can not pass the placental barrier). Fetomaternal bleeding in
the subsequent pregnancies results in the anamenstic reaction producing an Igg type of
antibody (small antibody that can pass the placental barrier).
Factors that affect this maternal response are inborn responsiveness of the mother (30% are
non responders), volume and rate of hemorrhage (as little as 0.1 ml is enough), and
presence of ABO incompatibility (reduces risk by 50 -75%).
The overall risk of isoimmunization of an Rh positive ABO compatible fetus is 16%.
Antibodies can be detected before the delivery of the first Rh positive fetus in 1% and in
another 8% it will be detected within 6 months of delivery and in another 8% the level is so
low that it cannot be detected until the early part of the second pregnancy.
In addition, for hemolytic disease of the newborn and hydrops fetalis to develop transfer of
the Igg type antibody and antibody mediated destruction of fetal red blood cells must occur.
The first neonate is usually spared but subsequent Rh positive fetuses are affected, extent
worsening with each pregnancy.
4. Effects on the fetus and the newborn
Hemolytic anemia develops, the extent of which depends on the amount of antibody. To
compensate for the ensuing anemia the fetal bone marrow and later the extramedullary sites
that produce RBC (liver, spleen and placenta) are called to produce red blood cells at fast
rate. This results in the appearance of young nucleated cells in the blood stream.
In severe cases even extramedullary hematopoiesis can not cope with the degree of
destruction. This results in progressive anemia which eventually leads to congestive heart
failure and tissue hypoxia. The liver parenchyma is replaced by hematopoeitic tissue. Serum
albumin falls as the result. Portal hypertension develops from obstruction of the portal veins.
The combination of these causes generalized edema of the fetus called hydrops fetalis.
Eventually fetal death occurs.
Before delivery the bilirubin, mainly of unconjugated type is cleared by the placenta.
Following the delivery of the fetus, increasing amounts of unconjugated bilirubin accumulate
in the neonatal circulation (because the limited capacity of the liver to clear). The
unconjugated bilirubin crosses the blood brain barrier and damages the basal ganglia to
cause kernicterus.
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The neonate may die of severe anemia or kernicterus.
5. Management of Rh negative unsensitized pregnancy
I. Identification of pregnancies at risk at the initial ANC visit
Determine blood group & Rh factor and indirect coombs test for antibody screening for all
pregnant mothers. The possible outcomes are
a. Rh positive with negative antibody screen – no further testing needed
b. Rh positive with positive antibody screen – consider atypical antibodies
c. Rh negative with positive antibody screen – manage as sensitized pregnancy
d. Rh negative with negative antibody screen – manage as unsensitized pregnancy
II. Management of unsensitized pregnancy
Determine the blood group and Rh factor of the partner
Repeat indirect coombs test at 28 weeks and at 36 weeks. If negative consider antepartum
prophylaxis with 300 micrograms of anti D gamma globulin at 28 weeks. If positive manage
as sensitized pregnancy.
Provide anti D prophylaxis in cases with amniocentesis, APH, external cephalic version.
Following delivery determine blood group of the newborn and antibody screening. If the
newborn is Rh negative no further treatment is needed. If antibody screen is positive monitor
the newborn for haemolysis and manage next pregnancy as sensitized. If newborn is Rh
negative and antibody screen is negative, provide anti D gamma globulin within 72 hours.
The usual dose is 300 micrograms but ideally should be determined by the extent of
fetomaternal hemorrhage. This is done by performing Kleihauer Betke test (acid elusion
test). For abortion of less than 12 weeks gestation the dose is 50 micrograms.
6. Management of sensitized mother
These women need specialized care with measurement of antibody levels in titers at
regular intervals, amniocentesis for bilirubin levels, serial ultrasound for detection of
hydrops and management of neonatal anemia and hyperbilirubinemia. Therefore, referral
of these women is the correct approach at health center level.
Important points about ABO hemolytic disease
· It occurs when the mother has group O blood (with anti-A and anti-B antibodies in her
serum) and fetus is group A, B or AB.
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· Unlike Rh isoimmunization, 40-50% of ABO incompatibilities occur in the first-born
infant.
· ABO hemolytic disease is primarily manifest following birth, when the infant becomes
jaundiced within the first 24 hours with a variable amount of anemia and
hyperbilirubinemia which is usually mild. Serious complications almost never occur.
· The management consists of measurement of bilirubin serially and provision of
phototherapy to the newborn.
Review Questions
1. Discuss the pathogenesis of Rh isoimmunization.
2. Outline the management of unsensitized Rh negative pregnancy.
3. Describe the important features of ABO hemolytic disease.
CHAPTER 13
COMMON MEDICAL DISORDERS IN PREGNANCY
Learning objectives
To enumerate the common medical disorders in pregnancy.
To describe the clinical features of each of the common medical disorders in pregnancy and
their causes.
To outline the management of each of the common medical disorders in pregnancy.
To describe the effect of each of the common medical disorders on the pregnant woman and
her child with their implications.
ANEMIA IN PREGNANCY
1.1. Definition:
Anemia during pregnancy is defined as a hemoglobin level of 11 g/dl or less (hemtocrite of <
33%) except during the second semester, when the cut-off point is reduced to 10.5 g/dl. It is
said to be severe if the hemoglobin is less than 8gm/dl.
1.2. Incidence and causes
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It affects approximately 5- 50% of pregnant women in tropics and < 2% of in developed
countries. It is ore severe in tropics. It is the leading cause of indirect maternal mortality and
morbidity. It is the most common hematological abnormality during pregnancy.
Majority are nutritional anemias. Iron deficiency anemia account for 80-95 % of nutritional
anemias during pregnancy. Megaloblastic anemias from folate and vitamin b 12 deficiency
account for only 3-4% of nutritional anemias. Other causes of anemia (hemoglobinopathies,
leukemia, hemolytic anemias anemia of chronic illness and the like) are not common during
pregnancy.
1.3. Pathophysiology of nutritional anemia
The requirement of iron during pregnancy is around 1000mg. (450mg for red blood cells and
uterine muscle, 270 mg for fetal iron, 170-200 mg for daily loss and 90 mg for placenta).
There are additional needs for blood loss during delivery (190 mg) and lactation (1mg/day).
Assuming the stores are adequate a pregnant woman average daily dietary requirement is
3.5 mg/day. Failure to meet this demand eventually ends up in anemia. The sequence of
events in the development of frank anemia is depletion of the stores followed by deficient
hematopoiesis (microcytic and hypochromic RBC with abnormal RBC indices) and finally
reduction in RBC production results in evidences of frank anemia (decreased hemtocrite and
pallor).
The predisposing factors for iron deficiency anemia are
Inadequate intake of iron: food taboos, poor dietary habit, low socioeconomic state
Low store at the beginning of pregnancy: short interval between pregnancies, excess
menustral flow, hookworm infestation
Blood loss during pregnancy: early and late pregnancy bleeding, hookworm
Increased demand: multiple pregnancy, chronic infections
1.4. Complications
Anemia is associated with adverse pregnancy outcome.
Fetal: spontaneous abortion, preterm delivery, low birth weight, intrauterine growth
restriction, stillbirth,
Maternal: congestive heart failure and pulmonary edema especially in labour and postpartum
period, postpartum hemorrhage, puerperal sepsis, delayed wound healing, apathy, increased
risk of other infections like tuberculosis
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Neonatal: anemia of infancy
1.5. Treatment
It depends on the cause, severity and the gestational age.
I. Iron deficiency anemia
Ferrous sulfate 300mg containing 60 mg elemental iron of which 10%is absorbed,
three times per day, orally. Continue treatment for 3 months after the hemoglobin
concentration returned to normal. Alternatives are ferrous fumarate and ferrous gluconate.
Follow up with weekly hemoglobin and reticulocyte determination should be done.
Parenteral route of treatment in cases of intolerance of oral route or refractory to treatment
by oral route, and for very severe anemia.
Indications for blood transfusion are presence of congestive heart failure, severe anemia with
hemoglobin of<4.4 gm/dl, anemia with sepsis and renal failure, anemic patient with
hemoglobin of <6-7gm/dl seen for the first time in labour, abortion or in the last 4 weeks of
pregnancy. Packed RBC should be used.
Underlying causes, if any (like hook worm, malaria and chronic illnesses), other than
nutritional deficiency, should be treated also.
II. Megaloblastic anemia
Folic acid 5 mg three times / day and continued at a dose of 5 mg / day for the rest of
pregnancy.
1.6. Prevention of anemia
improve diet and dietary habit, socioeconomic status
Prevent and treat hookworm (deworming) and malaria
Child spacing by family planning
Universal supplementation of iron and folic acid to all pregnant women throughout pregnancy
iron fortification of staple diet
2. CARDIAC DISEASE IN PREGNANCY
2.1. Introduction
A woman with a known cardiac illness can become pregnant or a healthy pregnant woman
can develop cardiac illness while pregnant. In a woman with a preexisting cardiac illness, the
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increased homodynamic burden of pregnancy, labor and delivery can aggravate the
symptoms of the illness and/or precipitate complications. The risk of congestive heart failure
is the highest around 24 weeks of gestation, labour and the immediate postpartum period.
During each uterine contraction in labor about 200-300 ml blood is squeezed from the
contracting uterine muscles, increasing the cardiac output by about 20%.
2.2. Significance
Cardiovascular diseases are the most important non-obstetric cause of disability and death
of pregnant women, occurring in 0.4-4% of pregnancies. The most common cardiovascular
disease that complicates pregnancy is rheumatic heart disease. The reported maternal
mortality rate ranges from 0.4% in patients with New York heart association classifications I
and II to 68%or higher among patients with class III and IV severity. Patients with valvular
heart disease may develop subacute infectious endocarditis. It is also associated with
adverse fetal outcome like spontaneous abortion, preterm labour, low birth weight, and
intrauterine fetal death.
2.3. Classification
The degree of functional disability due to cardiac disease is graded according to the New
York Heart Association classification as follows:
Class I: No symptoms limiting ordinary physical activity.
Class II : Slight limitation with mild to moderate activity with no symptoms at rest
Class III: Marked limitation with less than ordinary activity; dyspnea or pain on minimal
activity.
Class IV: Symptoms at rest or with minimal activity and symptoms of frank congestive heart
failure.
Note: With rare exceptions, women in class I and most in class II go through pregnancy
without morbidity. As much as possible patients in classes III and IV should avoid pregnancy.
Therapeutic abortion is an option in early pregnancy. If the pregnancy is continued,
prolonged hospitalization or bed rest will often be necessary. These women tolerate major
surgical procedures poorly.
2.4. Management
Once diagnosed, these patients should be referred for specialized care by obstetrician,
internist and neonatologist. The general principles in the management are:
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I. Antepartum
Bed rest
Moderate dietary restriction
Provision of diuretics (chlorothiazides are accepted) with potassium supplementation
Prophylactic digitalization
Frequent ANC for maternal and fetal monitoring
II. Intrapartum
Unless contraindicated vaginal route of delivery is preferred
Conduct labour and delivery in lateral decubitus position
Provide adequate pain relief
Restrict intravenous fluids
Provide oxygen with breathing mask along with continuous pulse oxymetery
Provide prophylaxis for SBE for those with structural lesions
Shorten the second stage by instrumental delivery
Do not use ergometrine in the third stage
Prevent postpartum pulmonary edema by keeping the woman in sitting position
Provide thrombus prophylaxis by early ambulation and/ or low dose aspirin
Note: A patient with a known heart disease should consult her physician before becoming
pregnant in order to determine the advisability and optimum timing for pregnancy. In a
pregnant woman with a cardiac disease:
Recognize the presence of preexisting cardiac diseases.
Assess the degree of disability
Understand the impact of the added homodynamic changes of pregnancy.
Anticipate, prevent, diagnose and treat complications such as arrhythmia, congestive heart
failure when they arise.
Advise the patient regarding discontinuation or continuation of the pregnancy and risk of
future pregnancies.
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3. INFECTIOUS DISEASES IN PREGNANCY
3.1. Tuberculosis in pregnancy
It is a commonly encountered medical problem in pregnancy. Its effects on pregnancy
include preterm delivery, intrauterine growth restriction and low birth weight which increase
the perinatal mortality by 6 fold.
Adverse outcome on pregnancy correlate with late diagnosis, incomplete or irregular
treatment and advanced disease.
Diagnosis and management is similar to nonpregnants. With the exception of streptomycin
and pyrazinamide, all the first-line antituberculous drugs are safe to be used during
pregnancy. Streptomycin causes congenital deafness in the new born. The safety of the use
of pyrazinamide during pregnancy is not ascertained. Therefore, drugs used for treatment of
tuberculosis include: isoniazid (INH), rifampicin and ethambutol. However, pyrazinamide can
be included into the regimen if there is drug resistance. (Refer to the module on tuberculosis
for further detail).
Neonatal Tuberculosis
Neonates, though rare, can get tuberculosis infection in utero if the mother is suffering from
active tuberculosis. The incidence of congenital infection increases if the mother is HIV
positive. The tuberculous lesions in the new born are usually found in the liver. This can be
prevented if the mother is properly treated while pregnant.
3.2. Malaria in pregnancy
Types
Stable malaria occurs in endemic areas where there is repeated infection since childhood.
Community immunity is well developed and epidemics do not occur. During pregnancy
immunity slackens resulting in increased parasitemia and relapse rate of dormant
exoerythrocytic stages. Episodes of malarial infection increase by three to four folds during
the latter two trimesters of pregnancy and two months postpartum. Severity of falicparum
malaria is increased.
Unstable malaria occurs in areas with intermittent transmission. Community immunity is
poorly developed and epidemics occur. Malarial attacks are severe and cerebral malaria is
common especially in nulliparous women.
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Effects
They are related to pyrexia, haemolysis, placental parasitization (in immune) and
transplacental infection (in nonimmune).
Maternal: increased number of attacks, anemia from folic acid deficiency induced by
haemolysis, cerebral malaria, puerperal pyrexia
Fetal: spontaneous abortion, preterm labour and prematurity, intrauterine growth restriction,
intrauterine fetal death (stillbirth), congenital malaria in nonimmune in few days after delivery
Diagnosis
In immune women constitutional symptoms are subtle. Non immune women present with
constitutional symptoms with fever and chills. Blood film identifying the plasmodium parasite
confirms the diagnosis.
Treatment
Once diagnosed, malaria should be treated aggressively. Severe forms need inpatient
treatment with parentral antimalarials. Drug of choice depends on the type of plasmodium
parasite and the degree of resistance in the community. Chloroquine, sulfadoxine-pyrimethamine,
mefloquine and quinine are safe to be used in pregnancy. For details refer to
modules on malaria.
Prophylaxis
This is given for nonimmune people traveling to endemic areas. The drug should be taken 1-
2 weeks before travel and continued for4 weeks after return. Depending on the pattern of
resistance, drugs like chloroquine, mefloquine or sulfadoxine-pyrimethamine can be used.
3.3. HIV infection and pregnancy
I. Epidemiology
Since its discovery in 1981, HIV/AIDS has become a serious health problem worldwide. The
problem is most prevalent in developing countries. 80% of HIV-infected women are of
childbearing age.
The prevalence of HIV infection among pregnant women attending antenatal care services in
East and Central Africa ranges from 20% to 30%. In Ethiopia it is 10% to 20%. HIV/AIDS is
now a common cause of death among young women, most importantly pregnant women.
AIDS related maternal deaths are increasing dramatically and are displacing common
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obstetric causes. It also increases childhood mortality directly as the result of childhood AIDS
or indirectly from neglect off orphans.
II. Effects of HIV on pregnancy
HIV infection is associated with increased adverse obstetric outcomes like spontaneous
abortion, preterm delivery, low birth weight and stillbirth. Another significant effect is mother
to child transmission of infection (MTCT), which is by far the largest source of HIV infection in
children. There is also increased maternal morbidity and mortality from intrapartum and
postpartum infection.
III. Effects of pregnancy on HIV
Pregnancy induced immune suppression accelerates the progress of HIV infection only in
women in late stages of the disease but not in asymptomatic HIV positive women. When
comparing changes in CD4 count/percentage over time, there is no difference between HIV-positive
pregnant and non-pregnant women, suggesting that pregnancy does not accelerate
decline in CD4 cells in asymptomatic carriers.
IV. Mother to Child Transmission (MTCT)
MTCT of HIV infection occurs during pregnancy (5-10%), delivery (10-20%) and through
breast feeding (10-20%). The overall rate of HIV transmission from an HIV positive mother to
her child is 25-50% In developed countries 15-25%). Factors affecting MTCT of HIV are
General factors: maternal viral load and CD4 counts (more in advanced disease and recent
infections), type of virus (HIV2 has 20 times risk than HIV1), treatment with antiretroviral
drugs (reduces MTCT by 50%)
Antenatal factors: prematurity, obstetric procedures (amniocentesis and external cephalic
version), obstetric complications (abruptio placenta and placenta previa), infections (malaria
and STI), vitamin A deficiency and smoking
Intrapartum factors: prolonged labour, chorioamnionitis, prolonged rupture of membranes
(risk increases by 2% every hour after 4 hours) invasive procedures (internal monitoring,
scalp sampling, operative vaginal delivery and episiotomy)
Note: elective caesarian section reduces risk but caesarian section done after labor
has started especially in the presence of rupture of membranes or prolonged labor
increases risk. Another problem with caesarian section is increased risk of
postpartum infection by 5-7 times.
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Breast feeding factors: cracked nipples, acute mastitis, neonatal oral thrush and other
gastrointestinal lesions, mixed feeding, duration of breast feeding of ore than 14- 16 weeks
V. Prevention of MTCT (PMTCT)
For effective PMTCT, a four pronged approach has been developed by WHO. These basic
components of comprehensive PMTCT are
I. Primary prevention of HIV in women:
Provision of VCCT for all women
Helping HIV negative women to remain HIV seronegative through risk reduction behaviors
(abstinence, limiting partners and safe se by use of condoms)
II. Prevention of unwanted pregnancy in HIV positive women:
Counseling about the effects of HIV on pregnancy, health of the mother, long-term health of
the mother and child and risk of transmission to the newborn
Provision of family planning services
III. Prevention/ reduction of transmission of HIV virus during pregnancy, childbirth and
breast feeding:
A. Antepartum:
Universal VCCT service for all pregnant women
Reduce viral load by short coarse antiretroviral therapy (niverapine 200 mg at the start of
labour to be repeated if not delivered in 48 hours and single dose 2 mg/ kg for the neonate
within 72 hours of delivery. If delivery occurs less than 1 hour after the maternal dose two
doses are given for the neonate one as soon after delivery as possible and the second dose
after 48-72 hours of the first dose). Other regimens include zidovudine, lamivudine,
combination of zidovudine and niverapine/ lamivudine and finally highly active antiretroviral
therapy (see below).
Additional measures: risk reduction behaviors including safe sex, treatment of nutritional
deficiencies and concomitant STI, prophylaxis for malaria and avoidance of smoking
Note: There may be no need to increase the number of visits unless there evidences
of obstetric complications and signs/symptoms of advanced infection (opportunistic
infection and other AIDS indicator illnesses).
B. Intrapartum
Improving obstetric practices to prevent avoidable exposure to the virus at birth
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Avoid prolonged rupture of membranes and prolonged labour by proper use of partograph
Avoid artificial rupture of membranes as long as labour is progressing well. If it is done
delivery has to occur within 4 hours. Some use anti septic preparation of the vagina when
rupture of membranes is more than 4 hours.
Avoid repeated pelvic examinations, internal monitoring of the fetus and fetal scalp blood
sampling
Treat chorioamnionitis aggressively
As much as possible avoid caesarian section after rupture of membranes. Provide
prophylactic antibiotics to the mother.
Avoid routine pubic hair shaving, unnecessary episiotomy or instrumental delivery
Prevent tears by controlled delivery of the fetus
Clamp the cord immediately after delivery. Cut the cord after pulsation stopped under light
gauze. Do not milk the cord towards the newborn
Avoid/ reduce suction by nasogastric tube. If needed do it gently. Provide universal neonatal
care to the neonate.
Apply universal precautions throughout
Educate about the infectiousness of the lochia and how to handle sanitary napkins.
C. Breast feeding
Modify infant feeding practices. Depending on the resources, two options: exclusive
replacement feeding and exclusive breast feeding for 6 months followed by abrupt
weaning. Ideally decision should be made during pregnancy and necessary preparations
made. Mixed feeding should be avoided.
IV. Care and support of the mother (PMTCT Plus):
Continued care of the mother after delivery by provision of antiretroviral drugs, treatment of
opportunistic infections
Social and economic support
Other drug regimens in PMTCT
I. Zidovudine: Antepartum: treatment is initiated at14-34 weeks and continued
throughout pregnancy, being administered 2-5 times per day, depending on the dose.
Intrapartum: zidovudine is given IV over 1 hour followed by continuous infusion until
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delivery. Postpartum: zidovudine is given orally to the newborn for the first 6 weeks of life,
beginning at 8-12 hours after birth.
II. Zidovudine/Lamivudine: Antepartum: Zidovudine and lamivudine given orally at the
onset of labor followed by Zidovudine orally every 3 hour until delivery with lamivudine
orally every 12 hours. Postpartum: Zidovudine orally every 12 hours with lamivudine
orally every 12 hours for 7 days
III. Zidovudine/Nevirapine: Intrapartum: Zidovudine IV bolus followed by continuous
infusion until delivery with nevirapine single oral dose at the onset of labor. Postpartum:
Zidovudine orally every 6 hours for 6 weeks with nevirapine single oral dose at age 48-72
hours
3.4. Urinary Problems in Pregnancy
I. Asymptomatic bacteruria
Definition and incidence
It is defined as presence of greater than 105 colony forming units (CFU) of bacteria of single
pathogen per ml of clean-catch midstream urine sample with no clinical symptoms of urinary
tract disease.
Asymptomatic bacteruria occurs in 7% of pregnant women (ranging from 2%-12%). The
predisposing conditions are reduced peristalsis and dilatation of the ureters and the bladder
causing incomplete emptying and stasis of urine and pregnancy induced glycosuria.
Significance
If untreated, about 25%-30% of patients with asymptomatic bacteruria will later develop
acute pyelonephritis as compared to only 2%-3% of patients who have been treated. It is
also associated with preterm labour and postpartum endometritis. Acute pyelonephritis is one
cause preterm birth and perinatal death.
Etiology
In 80 to 90% of cases the etiology is E coli, the other causes are Klebsiella, Proteus,
Pseudomonas, S saprophyticus and C trachomatis.
Diagnosis and management
Sine it has no symptoms and is associated with adverse obstetric outcome, routine urine
culture for all women is recommended in ANC. Once diagnosed al women with
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asymptomatic bacteruria should be treated with appropriate antibiotics. Urine culture should
be repeated to confirm cure.
Empirical treatment with antibiotics should be started until culture and sensitivity result is
ready. Commonly used antibiotics (since the most common pathogen is E coli) are:
amoxicillin, amoxicillin/clavulanate potassium, cephalexin, nitrofurantoin, trimethoprim-sulfamethoxazole
or one of the third generation cephalosporins. The antibiotic should be safe
to be used during pregnancy and given for duration of 10-14 days. Culture of urine should be
done 1-2 weeks after therapy is begun and monthly for the remainder of pregnancy.
Treatment failure can be due to resistance and patient non compliance.
II. Acute cystitis
It is the inflammation of the bladder in this case due to infection. The predisposing factors
and etiologic agents are similar with that of asymptomatic bacteruria.
Clinical features are urinary frequency, urgency, dysuria, suprapubic discomfort or pain,
and suprapubic tenderness. The urine may be cloudy and malodorous. Systemic symptoms
like nausea, vomiting, fever and chills are unusual.
Diagnosis is made by microscopic examination of urine (shows bacteria, leukocytes and red
blood ells) and urine culture.
Treatment: similar with that of asymptomatic bacteruria.
III. Acute pyelonephritis
Acute pyelonephritis is the infection of the renal pelvis and the kidneys. The single most
important predisposing factor for acute pyelonephritis during pregnancy is asymptomatic
bacteruria. The etiologic agents are similar with those of asymptomatic bacteruria and acute
cystitis. Acute pyelonephritis affects 1% - 2% of all pregnant women.
Clinical features generally develop rapidly over a few hours or a day. Symptoms include
fever (usually > 390C), shaking chills, nausea, vomiting, bilateral flank pain and possibly
diarrhea. Symptoms of cystitis may or may not be there. In some hematuria may be evident.
On physical examination, there is pyrexia and tachycardia along with costovertebral angle
tenderness on one or both sides.
Diagnosis is made by urine microscopy showing pyuria (in centrifuged urine >10 WBC per
high power field), bacteruria, hematuria (1-2 RBC in centrifuged urine or ≥5 RBC in
uncentrifuged urine per high power field) and leukocyte casts, leukocytosis (WBC
>15,000/mm3) with left shift and positive urine/blood cultures.
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Complications are septic shock, acute renal failure, preterm labour and low birth weight
baby.
Management: Admit for parentral antibiotics. Start high dose parentral antibiotic until the
patient is afebrile for 24-48 hours (usually 3-5 days) then continue orally for 7- 10 days.
Antibiotics are initially started empirically but later can be adjusted according to culture
results. (Examples: ampicillin 1 gm four times plus gentamycin 80mg three times a day or
ceftriaxone 1-2g daily).
Supportive care includes correction of dehydration, antipyretic agents as required for control
of fever and monitoring vital signs and urinary output.
4. DIABETES MELLITUS IN PREGNANCY
4.1. Definition
Diabetes mellitus is a chronic disorder of metabolism affecting carbohydrates, proteins, and
fats. It is characterized by an absolute or relative lack of insulin, hyperglycemia and
glycosuria. The worldwide incidence of diabetes mellitus during pregnancy is 1-4%.
4.2. Classification
I. Pregestational (overt) diabetes: This is diabetes existing before pregnancy. It is further
classified into:
Type I diabetes: It is also known as juvenile or insulin dependent diabetes mellitus. There is
autoimmune destruction of β-cells of the pancreas resulting in absolute lack of insulin in the
body. Patients require exogenous insulin for treatment and to prevent ketoacidosis.
Type II diabetes: It is also known as maturity-onset or non-insulin dependent diabetes
mellitus. In this type there is abnormal insulin secretion and insulin resistance in target
tissues. It is hereditary. Most patients are obese.
II. Gestational diabetes (GDM or Type III diabetes): This is defined as carbohydrate
intolerance of variable severity with onset or first recognition during pregnancy. This
definition applies regardless of whether or not insulin is used for treatment. “Gestational”
diabetes implies that this disorder is induced by pregnancy, perhaps due to exaggerated
physiologic changes in glucose metabolism. An alternative explanation is that gestational
diabetes is maturity-onset or type II unmasked or discovered during pregnancy. Actually,
some women with gestational diabetes have previously unrecognized overt diabetes.
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4.3. Diagnosis
I. Overt diabetes
Previous history of diabetes along with symptoms of polyuria polydypsia polyphagia and
weight loss and in long standing cases finding of signs of organ damage (retinopathy
nephropathy and atherosclerosis) suggest the diagnosis. It is confirmed by finding high
plasma glucose levels and / or glycosuria
II. Gestational diabetes mellitus
The process of diagnosis of gestational diabetes involves a two-step screening and
diagnostic glucose tests on patients with risk factors for gestational diabetes. Since 35-50 %
of women with gestational diabetes have no risk factors, it is wise to adopt universal
screening of all pregnant women.
A. Risk factors
Maternal age greater than 35 years
Bad obstetric history: recurrent abortion, previous unexplained stillbirth, previous macrosomic
(>4000g) infant, history of congenital malformed fetus, previous unexplained neonatal death,
history of polyhydramnios or PIH in multipara
History of pregnancy with GDM
Family history of diabetes mellitus in first degree relative
Obesity (>90 kg)
Recurrent urinary tract infection or vulvovaginal candidiasis
Persistent glycosuria.
B. Screening for GDM
Screening for GDM should be performed between 24 and 28 weeks by giving 50 gm glucose
orally and determining plasma glucose after 1 hour. Plasma glucose level of > 140 (135)
mg/dl is abnormal and mandates oral glucose tolerance test. If it is < 140 (135) mg/dl no
further test is needed.
C. Diagnostic test
Oral glucose tolerance test (OGTT) performed by administering 100gm of glucose after 8-
14hrs overnight fast and 3 days carbohydrate loading. Blood glucose is determined every
hour for three hours. It is abnormal if two or more of the following are found: (FBS > 95 mg/dl,
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1 hour plasma glucose > 180 mg/dl, 2hour plasma glucose > 155mg/dl, 3 hr plasma glucose
> 140 mg/dl).
4.4. Complications
Unlike GDM, over diabetes has significant impact on pregnancy outcome. The adverse
outcome depends on the degree of glucose control and to the intensity of the long term effect
of the diabetes on the mother’s health. Some of the effects are:
Fetal: spontaneous abortion, congenital malformation, intrauterine growth retardation,
polyhydramnios/ oligohydramnios, prematurity, macrosomia, sudden intrauterine fetal death
Maternal: preeclampsia, recurrent vulvovaginal candidiasis, urinary tract infection, operative
deliveries, worsening nephropathy and retinopathy, increased dose of insulin
Neonatal: hypoglycemia, hyaline membrane disease, hypocalcaemia, hyperbilirubinemia,
traumatic delivery of macrosomic neonate
Depending on the degree of hyperglycemia, the following are some of the adverse effects of
GDM.
Fetal: macrosomia, polyhydramnios, unexplained intrauterine fetal death, congenital
malformations
Maternal: preeclampsia, operative deliveries, Urinary tract infection, candidiasis, postpartum
endometritis,
4.5. Management
I. Overt diabetes
Preconception: Counseling on the complications of diabetes, evaluation of the diabetic
status, achieving adequate glycemic control.
Pregnancy: Target glucose levels to be achieved during pregnancy are fasting glucose of
105 g/ dl (60-90mg/dl preferable), postprandial glucose <130mg/dl at 1 hr or 120mg/dl at
2hrs without development of significant hypoglycemia (plasma glucose <70mg/dL) during the
hours of sleep.
This is achieved by multiple insulin injection adjusted to bring glycemic control, dietary
adjustment and/ or exercises. Optimum glucose monitoring assured by repeated self glucose
determination. Insulin requirement increases during pregnancy to reach maximum at 16-18
weeks. Fetal growth and well being is followed by fundal height, kick chart, ultrasound and
other fetal wellbeing tests.
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Delivery: If the glucose control is optimal and the fetal condition is reassuring, delivery can
be accomplished near term. In the presence of arrested fetal growth, intrauterine growth
restriction, abnormal fetal well being tests, maternal complications like severe preeclampsia
and mature fetus delivery should be accomplished either by induction or caesarian section.
Intrapartum glycemic control is achieved by regular insulin and hourly monitoring of the blood
glucose levels.
Postpartum: Insulin requirements drop drastically. Prevent neonatal complications like
hypoglycemia (early feeding).
II. Gestational diabetes
Glycemic control is achieved in most cases by dietary adjustment. If this fails insulin in low
doses is used. Insulin is indicated when FBS>95mg/dL and 1 hr postprandial glucose
concentration > 120mg/dL on two or more occasions within a two weeks interval despite
attempted dietary control. Fetal growth and well being monitoring is conducted as for overt
diabetes.
Note: Oral hypoglycemic agents are contraindicated during pregnancy.
4.6. Postpartum consequence of GDM
There is a 50% likelihood of women with GDM of developing overt diabetes within 20 years
of delivery. If fasting hyperglycemia develops during pregnancy, diabetes is more likely to
persist postpartum. Therefore, it is recommended that women diagnosed to have GDM
undergo evaluation with 75-g oral glucose tolerance test after 6 to 12 weeks after delivery.
Fasting blood sugar ≥140 mg/dl and 2 hr plasma glucose level ≥ 200mg/dl in this 75-g oral
glucose tolerance test indicate overt diabetes.
Review Questions
1. Discuss the causes and consequences of anemia during pregnancy.
2. Describe classification and general management principles of cardiac disease in
pregnancy.
3. Discuss the measures taken to prevent MTCT.
4. Discuss the diagnosis and complications of asymptomatic bacteruria.
5. Discuss the risk factors and screening methods of GDM.
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References
1. DeCherney AH, Pernoll ML Current. Obstetrics and Gynecologic diagnosis and
treatment, 8th edition, 1994.
2. Lawson J. B, Stewart D. B, Obstetrics and Gynecology in the Tropics and developing
countries
3. Scott JR., DiSaia PJ, Hammond CB, Spellacy WN: Danforth’s obstetrics and Gynecology,
8th edition, 1999.
4. Novak’s text of Obstetrics & Gynecology, 10th edition, 1981.
5. Addis Ababa University faculty of medicine department of Obstetrics and Gynecology:
Guideline for management of obstetric and gynecologic problems, 1st edition, 2003.
6. Bennett V.Ruth and Brown Linda K.: MYLES text book for mid wives, 13th edition
7. Llewellyn Jones D, Fundamentals of Obstetrics and Gynecology, Volume 1, Fifth edition,
1990
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126. Obstetrics and Gynecology
8. Kenneth R. Niswander, Manual of Obstetrics, diagnosis and therapy, 1st edition, 1982
9. John Cook, Surgery at district hospital, Obstetrics and Gynecology 1991
10. Dreissen F, Obstetric problems, A practical manual, 1991
11. WHO, Department of reproductive health and research, integrated management of
pregnancy and childbirth. Managing complications in pregnancy and childbirth. A guide for
midwives and doctors, 8.
12. MOH/ FHD, Technical Guidelines in managing maternal and new born care
13 Cunningham F. Gary et. al, Williams Obstetrics,20th edition, 1993
14. King M, Bews P, Karins, Thornton J: Primary surgery, Volume 1 (Non trauma); Oxford
medical publication, 1990
15. WHO, Safe Abortion: Technical and Policy Guidance for Health Systems, 2003.
16. WHO, Clinical Management of Abortion Complications: A Practical Guide., 1994.
17. Addis Ababa University, Faculty of Medicine, Department of Obstetrics and Gynecology,
The Management of Abortion and Post Abortion Care. September 2001.
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PART II
NORMAL AND ABNORMAL LABOUR
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CHAPTER 14
PHYSIOLOGY AND MANAGEMENT OF NORMAL LABOUR
Learning objectives
· To define true labour and describe its difference from false labour
· To describe the stages of labour
· To describe cardinal movements in the mechanism of labour
· To discuss the management of normal labour
· To list the types and complications of episiotomy
I. Definitions
True labour (parturition) is a continuous process in which progressive regular uterine
contractions result in the expulsion of the products of conception from the uterus through the
birth canal after progressive effacement and dilatation of the cervix.
Labour can be preterm (if it starts before 37 completed weeks) or term (if it starts between
37- 42 weeks) or post term (if it starts after 42 weeks). It can be spontaneous or induced.
Labour is said to be normal only if the following are met. These are:
· It starts spontaneously
· It starts at term (37- 42 completed weeks)
· The fetus presents by vertex
· Delivery is effected vaginally spontaneously
· It ends in a birth of healthy newborn with minimal morbidity
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False labour is a painless irregular uterine contraction occurring in the last 4-8 weeks of
gestation and which doesn't result in cervical dilatation and effacement.
Differences between true labour and false labour
false labour true labour
contractions occur at irregular intervals contractions occur at regular intervals
with time contractions remain the same or
decreases in intensity, frequency
with time contractions increase in intensity,
frequency and duration
contractions disappear with analgesics contractions persist despite analgesics
lower abdominal and back pain present only lower abdominal discomfort present
can occur in the last trimester occurs when labour commences
there is no cervical effacement and
dilatation
there is progressive cervical dilatation and
effacement
occurs at night occurs at any time
Braxton-hicks contraction is an irregular painless contraction which occurs in the last
trimester of pregnancy with no effect on the cervix.
Lightening is a sensation (the fetus falling down into the pelvis and emptiness in the upper
abdomen) felt by most primigravidas in the last weeks of pregnancy prior to the onset of
labour. It denotes engagement of the fetal head.
II. Stages of Labour
Even though labour is a continuous process, for the sake of management, it is classified into
the following four stages.
1. First stage of labour
It extends from the onset of regular uterine contractions to full cervical dilatation. It
is further subdivided into two phases the latent phase and the active phase. The latent
phase extends from the onset of labour to three to four centimeters of cervical dilatation.
The active phase extends from three centimeters to full cervical dilatation (10
centimeters). The active phase has acceleration phase, phase of maximal
slope (average rate of cervical dilatation is greater than 1.2 cm/hr for primigravida
and 1.5 cm/hr for multigravida) and deceleration phase.
2. Second stage of labour
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It extends from full cervical dilatation to delivery of the fetus. It is characterized by
more frequent and strong contractions. In addition to uterine contractions maternal
voluntary efforts play major role. Descent is more during this stage.
3. Third stage of labour
It extends from the delivery of the fetus to the delivery of the placenta and
membranes. Its duration is equal in multiparas and primiparas. In majority it lasts 15
minutes.
4. Fourth stage of labour
It extends from the delivery of the placenta and membranes to one hour
postpartum.
Mean duration of primigravida and multigravida
Stage of labour Primigravida Multigravida Factors
Latent first stage 8 hours 4-6 hours parity, uterine contraction, ability of
the cervix to dilate, feto pelvic
diameter, presentation, position
Active first stage 6- 8 hours 4-6 hours
Second stage 1 hour 20-30 minutes parity, contraction, soft tissue
resistance, feto pelvic diameter,
presentation, position, maternal
effort
Third stage 15-30 minute 15-30 minutes speed of separation of placenta
Rate of cervical
1.2 cm/ hr 1.5 cm/ hr -
dilatation
Rate of descent 1 cm/ hr 2 cm/ hr -
III. Theories for initiation of labour (parturition)
Many theories have been proposed over the years to explain labour and delivery. The
physiological processes in human pregnancy that results in initiation of labour and onset of
labor are not defined. The mother, fetus and placenta contribute to the initiation of labour.
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IV. The mechanism of labour
The mechanism of labour refers to the changes in the positions of the presenting part during
its passage in the birth canal. It is a process of adaptation in which the smallest diameter of
the presenting part is presented to the various portions of the pelvis. The major force for
these changes comes from uterine contractions.
There are seven cardinal movements in the mechanism of labour.
1. Engagement: is said to occur when the largest diameter of the presenting part passes the
plane of the pelvic inlet. For occiput presentation the largest diameter is the biparital diameter
(BPD). In nulliparous engagement occurs in the last weeks of pregnancy and is experienced
as lightening by the mother. But in multiparous this usually occurs at the onset of labour.
Engagement occurs in occiput transverse or oblique position.
2. Descent: occurs in discontinuous manner. In women with engaged head descent starts in
late first stage or in the second stage. In others it starts with engagement with the greatest
rate occurring in the deceleration phase.
3 Flexion occurs as a passive movement resulting from the resistance of the soft tissues of
the pelvis. Flexion ensures presentation of smaller diameter of the fetus to birth canal. It is
important for both engagement and descent.
4. Internal Rotation occurs at the pelvic floor at the level of the ischial spines. The sagittal
suture rotates 450 (in left or right occipito anterior position) or 900 (in left or right occipito
transverse positions) so that the sagittal suture lies in the anteroposterior diameter. It occurs
because of the force exerted by the uterine contraction and resistance created by the v-shaped
levator ani muscles. This helps the head to pass the ischial spines.
5. Extension: After further descent and flexion the head reaches the introitus. Delivery of
the head is then achieved by extension where the lower border of the symphysis acts as the
fulcrum for the occiput and the fetal face sweeps the perineum to be delivered. Following
delivery of the head, the head restitutes to the oblique lateral position.
6. External rotation is evidenced when the face starts to look to the side. This indicates
internal rotation of the shoulders.
7. Lateral flexion of the body or expulsion results in the delivery of the anterior shoulder
under the symphysis to be followed by the posterior.
One can remember the cardinal movements by the mnemonic Every Decent Family In
Europe Eats Eggs.
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V. Physiologic changes in labour
Contractions increase in intensity and frequecy as labour progresses. With contractions, the
uterus differentiates into an active upper segment (which gets progressively thicker) and a
passive lower segment (which gets progressively thinner).
In response to the increased hydrostatic pressure of the amniotic fluid and direct pressure of
the fetus, the cervix initially undergoes effacement (taking up of the cervix into the lower
segment so that 3 centimeters long cervix becomes a circular orifice with paper thin edges)
and later dilatation (from closed state to 10 centimeters).
The fetal head descends in the birth canal dictated by the mechanisms of labour. Pressure
over the leading part of the head results in edematous swelling, called caput succedaneum.
Overlapping of the fetal skull bones called molding may accompany the caput.
In the second stage, uterine contractions are intense and frequent. At this time most will have
the urge to defecate and vomiting along with appearance of beads of sweat on the face.
During this stage the most important force to expel the fetus is maternal voluntary expulsive
force.
In the third stage, sudden reduction in uterine cavity results in decrease in the surface area
of the placental attachment. The placenta becomes thicker and eventually gives way at the
decidua spogiosa. Separation proceeds through this layer until it is complete. Then, the
placenta is delivered by the help of uterine contraction and maternal effort. There are two
mechanisms of separation: Schueltz method (central separation with clot behind so that the
placenta is delivered by the fetal side like an inverted umbrella) and Mathew-
Dunken method (peripheral separation with blood escaping ahead of the placenta so that the
placenta is delivered sideways by the maternal side).
VI. Diagnosis of labour
Labour can be diagnosed if three of the following present:
· Presence of regular painful contractions at least 2 in 10 minutes
· Bloody show which is expulsion of the cervical mucus plug of pregnancy along with
some blood
· Cervical dilatation of 3 cm. or more which is progressive
· Cervical effacement of 80% or more
VII. Management of normal labour
1. Major objectives
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· Prevention minimize infection which could be intrinsic or extrinsic
· Prevent dehydration and ketosis
· Prevent or minimize trauma to the fetus and the mother
· Provide pain relief
· Avoid asphyxia to the newborn
· Prevent postpartum hemorrhage
2. Initial assessment
Its objective is to diagnose labour and its stage and identify significant problems. This is done
by brief history and physical examination and appropriate investigations (mainly hemtocrite
and urine protein). If available, antenatal data should be reviewed.
In the history one should get information on time of onset of contractions, status of fetal
membranes and time of rupture, presence/absence of vaginal bleeding and show, presence
and quality of fetal movement, symptoms of severe preeclampsia (head ache, blurring of
vision, epigastric pain), presence of fever, history of allergy, time and content of last ingestion
of food or fluid and use of any medications. Information should also be gathered on the
presence of ANC and significant problems during pregnancy. Review of past obstetric
medical, surgical, personal, social and family history must be made. (Refer to chapter 2)
In the physical examination, special attention should be given to vital signs, weight, signs of
anemia and dehydration, fetal position and presentation (proper Leopold’s maneuver), fetal
heart rate and its pattern, frequency, duration and quality of uterine contractions and
estimation of fetal weight. If there is no contraindication digital pelvic examination must be
done to assess degree of cervical effacement and dilatation, status of membrane and the
color of the liquor, the presenting part , its position and station, in cephalic presentation
degree of caput and molding and when indicated clinical pelvimetry (pelvic inlet, mid pelvis,
pelvic outlet).
Correct diagnosis and identification of high risk patient is made for adequate surveillance
through out labour and delivery.
3. Subsequent management
This depends on the stage of labour and identified problems.
3.1. First stage of labour
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The woman is admitted to the delivery ward. Ambulation can be allowed except in those with
ruptured membranes or having vaginal bleeding or are sedated. Left lateral position should
be adopted while lying in bed. She should be allowed to take sips of fluid, but not solid diet.
Parenteral fluids are reserved for those with vomiting or have prolonged labour of more than
12 hours. Routine use of cleansing enema and pubic hair shaving are not recommended.
Monitoring of labour has the following components (refer to annex 2 for partograph).
· Monitoring the fetal condition by auscultation of the fetal heart beat every 30 minutes
(for high risk every 15 minutes) for 1 minute after the end of contraction
· Monitoring the maternal condition by taking the vital signs every 1-2 hours (more
frequent in high risk woman) and measuring the urine output
· Monitoring the progress of labour by assessing uterine contraction for 10 minutes
every 30 minutes and cervical dilatation (and decent of the presenting part) every 4
hours. Vaginal examination is made every 4 hours to assess cervical dilatation,
station, degree of caput and molding and status and color of liquor. Vaginal
examination has to be done at any time following rupture of the membranes or if there
is unexplained fetal distress or if second stage is suspected.
3. 2. Second stage of labour
· Position the woman in lateral recumbent or lithotomy position with the knees
supported
· Monitor vital signs more frequently ( every 30 minutes to 1 hour)
· Fetal heart rate is checked every 15 minutes (if high risk every 5 minutes) looking
for late decelerations which is common (strong contractions, premature separation,
tightening of loops of cord)
· Vaginal examination is performed frequently. Prepare for delivery when the head
crowns and perineum bulges. If needed, perform episiotomy.
· Clean any feces that soil the perineum with sponges soaked with dilute soap
solution
· Deliver the fetus in controlled way. Deliver the head slowly. This is facilitated by
using modified Ritegen’s maneuver (gentle upward pressure at the chin thigh the
perineum just in front of the coccyx). Check for nuchal cord. If present slip it over
the head or cut it after double clamping. Suction any fluid from the nose and mouth
by soft rubber suction bulb or catheter. After external rotation, apply gentle
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135. Obstetrics and Gynecology
downward traction by holding to the sides of the head to deliver the anterior
shoulder. As soon as the anterior shoulder slips under the symphysis apply
upward traction to deliver the posterior shoulder.
· Provide immediate neonatal care. Clamp the cord after 15- 20 seconds by two
clamps placed 4-5 centimeters from the fetal abdomen and cut the cord using
sterile scissors. Later tie the cord tightly. Airway cleared of blood and amniotic fluid
by soft suction bulb or catheter. Dry the baby, wrap with blanket and put under
radiant heat. Examine for gross malformations and take Apgar score.
3. 3. Third stage of labour
A. Expectant or traditional method: controlled cord traction
· Determine the height and consistency of the uterus and assess the degree of bleeding.
Until the signs of placental separation are observed, frequently assess the tone but do
not massage
· When the signs of placental separation (gush of blood from the vagina, lengthening of the
cord, uterus becomes globular and rises in the abdomen) are observed, deliver the
placenta by controlled cord traction using either
1. Pastore technique: Stand on the patient’s left. Hold the fundus by the right
hand and put the left hand superior to the symphysis to prevent the uterus coming down.
If signs of placental separation noticed, massage the fundus gently to let the placenta
into the vaginal canal.
2. Modified Brandt-Andrews technique: This controlled cord traction with the
left hand superior to the symphysis to support the uterus.
Credes manuvoere of delivering the placenta (traction of the cord with
concomitant fundal pressure) is an abandoned technique that predisposes to uterine
inversion.
After delivery of the placenta give uterotonic drugs as described below
B. Active third stage management
It is universally recommended method of management of the third stage for all women. Its
components are:
· Secure an intravenous line; get blood for hemtocrite and blood group and cross
match.
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136. Obstetrics and Gynecology
· Depending on the presenting part and twin (in vertex: after the delivery of the anterior
shoulder, in breech immediately after delivery of the fetus, in twins after the delivery
of both fetuses) give uterotonic as below:
1. Oxytocin: 10 IU intramuscular or 10-20 IU added in 1000 ml of IV fluids to run
over 1 hour or
2. Ergometrine 0.2-0.5 mg intravenous slowly if not
contraindicated.
· Apply controlled cord traction without waiting for signs of placental separation. If the
placenta is not delivered within 6-10 minutes perform manual removal of the placenta.
C. Subsequent management
· Examine the placenta, cord and the membranes for completeness and
abnormalities. If incomplete or if excessive bleeding occurs perform intrauterine
exploration
· Examine the genital tract for laceration
· If performed, repair episiotomy
3.4. Fourth Stage of labour:
It is a critical stage of labour where most maternal deaths occur.
· Monitoring of maternal vital signs at least every 30 minutes (blood pressure must be
more than 90/60 mmhg and pulse rate must be less than 90/ minute)
· Examination of the uterus for its tone and size (it should be firmly contracted and at
the level of the umbilicus)
· Inspect the vulva for bleeding and hematoma
EPISIOTOMY
Episiotomy (periniotomy) is an intentional incision made into the perineum with an objective
of widening the vulva to allow easy passage of the fetus. The common types of episiotomy
are midline (median) and mediolateral, each with its own advantages and disadvantages
(see table below).
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137. Obstetrics and Gynecology
Median episiotomy is an incision made vertically in the midline of perineum over the
perineal raphae starting at the posterior fourchette and ends just anterior to the anal
sphincter.
Mediolateral episiotomy is an incision made at an angle of 450 from the midline beginning
at the midpoint on the posterior fourchette.
Medial Mediolateral
Technically easier to make and repair relatively difficult
Healing better Less
Blood loss less more
Dysparunia less more
Anatomic end result Better Less satisfactory
Extension into the rectum relatively more common rare
risk of rectovaginal fistula higher lower
Routine use of episiotomy is not advisable. Episiotomy should only be done in conditions
where perineal tear is imminent or likely. Such conditions include macrosomia, tight
perineum, breech delivery, shoulder dystocia, instrumental deliveries especially forceps
delivery and destructive deliveries.
Procedure
I. Incision of episiotomy
Infiltrate 5 - 10 ml of local anesthetic agent such as 1% lidocaine into the intended site of
episiotomy. Insert the needle at posterior fourchette and give the local anesthetic in fan
manner. Perform the incision, preferably when the perineum is thinned out and the
presenting part has crowned, by sharp tissue scissors in one go.
II. Repair of Episiotomy
After the delivery of the placenta, insert a rolled vaginal pad and inspect the episiotomy site
for extension. Identify the apex. Start suturing 0.5-1 centimeters above the apex using
chromic 2/0 catgut. Suture the vaginal mucosa continuously upto the hymen, the perineal
muscles by 2-3 interrupted sutures and the perineal skin by interrupted sutures. Perform
rectal examination to check for any sutures that may have passed (If found remove the
suture). Remove any vaginal pad.
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138. Obstetrics and Gynecology
Proper anatomic approximation of tissues, careful handling of tissues and proper hemostasis
are essential for success of the repair.
Subsequent care
The episiotomy wound should be cleaned with plain water and soap at least once or twice a
day and after voiding or defecation. Cool sitz bath can be used for relief of the pain. Simple
analgesics like parcetamol relieve the pain. Increasing swelling, persistent/ increasing pain
and offensive discharge call for inspection of the episiotomy.
Complications
· Extensions to upper vagina and even the cervix causing PPH
· Extensions to the anal sphincter and rectum
· Episiotomy site hematoma manifests with increasing swelling and pain in the first
48 hours. The site must be opened, bleeding points identified and ligated and
wound is then resutured.
· Episiotomy site infection manifests with increasing pain and swelling along with
offensive discharge usually occurring after the third day. Management includes
removal of sutures and drainage, wound cleaning and debridement and later
secondary closure. Antibiotics are needed only if there are signs of systemic
infection.
· Episiotomy breakdown/ dehiscence
· Rectovaginal fistula and anal incontinence
· Dysparunia from vulvar stenosis
· Gaping vulva
Review Questions
1. Define episiotomy
2. Discuss the types of episiotomy with their advantages and disadvantages
3. List the steps of making an episiotomy and repairing it
4. List the complications of episiotomy and their management
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139. Obstetrics and Gynecology
CHAPTER 15
INDUCTION / AUGUMENTATION OF LABOR
Learning Objectives
To define induction and augmentation of labor
To list indications for induction of labor
To list contraindications for induction of labor
To out line the steps in induction of labor
1. Definition
Induction of labor is initiation (stimulation) of uterine contraction artificially for the purpose
of delivering the fetus after the fetus has reached viability (after the 28th week of gestation). It
can be elective (planned) or emergency.
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140. Obstetrics and Gynecology
Augmentation of labor is enhancing uterine contractions that are inadequate to allow
normal progress of labour.
2. Indications
The decision to induce labor is largely governed by the assessment of obstetric balance. The
three factors that should be considered are
The risk if the pregnancy continues
The risk if the pregnancy is interrupted and
The hazards of induced labour
Because of associated risks, induction of labour should be performed only upon specific
maternal or fetal indications. The following are common indications for induction of labor (not
inclusive):
Hypertensive disorders of pregnancy
Antepartum hemorrhage from abruptio placenta and some types of placenta previa
Post term pregnancy
Intrauterine fetal death and intrauterine growth restriction
Premature rupture of membranes
Polyhydramnios and oligohydramnios
Gross congenital malformations incompatible with life
Recurrent intrauterine fetal death at term
Rh isoimmunization
Medical disorders like diabetes mellitus, chronic hypertension, cardiac diseases
3. Contraindications
I. Absolute contra indications
Cephalopelvic disproportion more than border line (macrosomia or contracted pelvis)
Transverse or oblique lie, footling breech
Previous history of uterine surgery like classical caesarian section, two or lower segment
caesarian section, myomectomy entering the endometrial cavity
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141. Obstetrics and Gynecology
Diagnosed major placenta previa
Extensive vaginal plastic operations like repaired fistulas or pelvic tumors obstructing delivery
like cervical cancer and tumor previa
Cord presentation
Abnormal fetal heart rate pattern
Absence of caesarian section facility
II. Relative contraindications
Elderly primigravida or grand multiparity or
Uterine over distention from polyhydramnios or multiple pregnancy
One lower segment caesarian section
Frank breech
These conditions require internal or external continuous monitoring of uterine
contractions and the fetal heart beat. In the absence of such monitoring, they become
absolute contraindications.
Unfavorable cervix is another relative contraindication especially for elective induction.
Favorability of the cervix for induction is evaluated by pelvic examination to assess the
Bishop score. Bishop score of more than eight is taken as favorable for elective induction.
Cervix is said to be unfavorable if the score is lees than five. The chance of vaginal
delivery is guarded in unfavorable cervix.
The Bishop Score
Factor
Rating
0 1 2 3
Dilation (cm) Closed 1-2 3-4 >5
Effacement (%) 0-30 40-50 60-70 >80
Station -3 -2 -1,0 +1,+2
Cervical consistently Firm Medium Soft -
Position of cervix Posterior Midposition Anterior -
4. Prerequisites
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Presence of clear indication
No contraindication
Presence of caesarian section facility
For elective induction screening for iatrogenic prematurity
Ripening of the cervix using prostaglandins or folley catheter.
5. Methods of induction
5.1. Medical induction – Intravenous oxytocin administration
The goal of oxytocin induction is to get sufficient (adequate) contractions without causing
hyperstimulation and fetal distress.
The principles of oxytocin induction are
Use oxytocin diluted in balanced salt solution or 5% dextrose in water as continuous
intravenous infusion
It has to be started from the minimum dose capable of causing contractions and increased
every 30- 40 minutes until adequate contraction is achieved or hyperstimulation and fetal
distress occurs or maximum dose is reached.
Continuous bed side attendance by a trained health professional should be provided
Close monitoring of uterine contractions and fetal heart beat (intermittently or continuously)
should be done
If hyperstimulation or fetal distress occurs discontinue the infusion
Complications of intravenous oxytocin are uterine hyperstimulation (more than 5
contractions in 10 minutes or contractions that last more than 1 minute) and fetal distress,
uterine rupture, water intoxication from antidiuretic effect of oxytocin if high dose is used
for prolonged periods, congestive heart failure from fluid overload and atonic PPH.
Different protocols to administer oxytocin are in use. Depending on the available
resources, some use high dose regimen while others use low dose. In our country the
low dose regimen is used.
Add 5 IU (for primigravida) or 2 IU (for multiparas) of pitocin in 1000 cc of 5%
dextrose in water. Start with 10 drops/ minute and double the drop rate every 20
minutes until 3-4 contractions each lasting 40- 60 seconds is achieved.
Rate in drops/min Pitocin in milli units/minute
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Primipara Multipara
10 2.5 1
20 5 2
40 10 4
80 20 8
If adequate contraction is not achieved, add another 5 IU (for primigravida) or 2
IU (for multipara) of pitocin into the same bag of intravenous fluid. Start with 40 drops/
minute and proceed as above.
Rate in drops/min Pitocin in milli units/minute
Primipara Multipara
40 20 8
80 40 16
If adequate contraction is not achieved, add 5 IU ( for primigravida) or 2 IU (for
multipara) of pitocin for multipara into the same bag. Start with 40 drops/ minute and
proceed as above.
Rate in drops/min Pitocin in milli units/min
Primipara Multipara
40 40 16
60 60 24
80 80 80
Maintain the drop rate that brought adequate contractions till delivery and
continue for one hour after delivery.
Note: For augmentation the same regimen using half the dose of the pitocin
used for induction.
5.2. Surgical induction - Artificial rupture of the membranes (ARM)
ARM stimulates labour mainly by initiating by release of prostaglandins from the
membranes.
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Contraindications for ARM are high (floating) presenting part, abnormal lie and
presentation, cord presentation, intrauterine fetal death, active genital herpes, maternal
HIV infection and history of unidentified APH.
Complications of ARM are umbilical cord prolapse and compression, chorioamnionitis,
abruptio placenta, adverse changes in fetal position and transmission of infection to the
fetus (HIV and genital herpes). Rare complications are amniotic fluid embolism and
rupture of vasa previa.
Procedure can be done either before or sometime after starting medical induction.
Discuss the procedure to the mother.
Check fetal heart rate pattern,
Wear sterile gloves and clean the vulva with antiseptic solution.
Perform pelvic examination and check the presenting part, the station of the head and for
cord.
Introduce one or two fingers through the cervix and pass Kocher forceps along side the
fingers towards the fore waters.
Hook or scratch the membranes and gently turn it to rupture the membranes. Allow the liquor
to drain slowly so that the head settles down.
Check thoroughly for the cord and note the color of the liquor.
Remove the fingers from the vagina and check the fetal heart for any variability.
If there is no adequate contraction in 1- 2 hours start oxytocin.
Give prophylactic antibiotics if not delivered in 12 hours.
5.3. Stripping of the membranes
6. Conduct of induction
Document the indication
Obtain informed consent after discussing about the indication, the methods, and risks
including the possibility of caesarian section
Thorough evaluation of the mother (to exclude contraindications and detect medical
problems).
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For elective induction, if there is unfavorable cervix, use cervical ripening drugs the day
before. Start induction early in the morning. Emergency induction should be started at any
time of the day.
Start induction using either medical or surgical method or combination of these methods as
described above.
Monitor induction by following dose of oxytocin, vital signs every 1 hour, uterine contractions
every 30 minutes, fetal heart beat every 20- 30 minutes, pelvic examination for cervical
dilatation and station every 4 hours, input output chart and urine output.
If labour starts follow with partograph. If the patient develops tetanic type of contraction, stop
the pitocin drip, sedate the patient and consider cesarean section. If the patient is not in
established labour after 6 hours of maximum dose of pitocin, the induction is said to have
failed.
Antibiotics cover when membranes are ruptured for more than 12 hours. Continue pitocin
drip until 1 hour after delivery.
t
7. Complications
Besides the complications of oxytocin and ARM, failure of induction and prematurity
(known or missed) are other complications.
Review questions
Define induction of labor
Outline the steps in ARM
List the maternal and fetal contraindications for induction of labor
List the maternal and fetal complications of induction of labor
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CHAPTER 16
OPERATIVE DELIVERIES
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Learning Objectives
To describe the parts of the obstetrics forceps and vacuum extractor
To describe the classification of forceps delivery
To list the indications, prerequisites and complications of instrumental deliveries.
To name the types, prerequisites and complications of destructive deliveries
To describe the major types of caesarian section with their advantages and disadvantages
To list the major complications of caesarian section
INSTRUMENTAL DELIVERY
Forceps delivery and vacuum delivery constitute instrumental deliveries. These are
techniques used to assist a laboring mother mostly in the second stage of labour. Except for
some variations the indications, prerequisites and complications of these procedures are
similar. They are entirely different in the type of instruments and the technique used to apply
the instruments.
1. Forceps delivery
Forceps delivery is a means of extracting the fetus with the aid of paired metallic instrument
called obstetric forceps.
1.1. Description of obstetric forceps
The obstetric forceps consists of two matched parts that articulate or "lock". It is designed to
fit to the sides of the fetal head with primary functions of traction, compression and in some
cases rotation of the fetal head. Each part of the obstetric forceps is composed of a blade,
shank, lock and the handle.
The blade, which may be fenestrated or solid, possesses two curves: the cephalic curve,
which permits the instrument to fit accurately to the sides of the fetal head and the pelvic
curve, which fits the curved axis of the maternal pelvis. The blades are referred to as left
blade and right blade according to the side of mother's pelvis on which they lie after
application. After articulation the left blade is held by left hand and the right blade is held by
the right hand of the operator. The shank could be short or long depending on the type of
forceps. The shanks are either overlapping or separate. The two blades articulate at the
lock. Most obstetric forceps possess a fixed type of lock (either English type or French type)
where as very few like the Kielland forceps possess sliding type lock. The lock leads to the
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most proximal parts of the forceps which are the shoulder and the handle where the hand
of the operator rests to apply traction.
1.2. Classification of Forceps Delivery
Based on the station and the degree of rotation of the head, forceps delivery is classified as
Outlet forceps: head has reached the pelvic floor and is visible at the vulva with the sagittal
suture in anteroposterior or one of the oblique diameters
Low forceps: head at station +2 cm or lower but has not reached pelvic floor
Mid forceps: head is engaged but station is above +2. It should be done as a trial of forceps
in an operating theatre.
High forceps: head is above station 0 and is not engaged. It is obsolete in modern obstetrics.
1.3. Indications
Fetal distress in the second stage of labor
Prolonged second stage of labor: inefficient uterine contraction or maternal exhaustion or
malpositions.
Maternal conditions which need shortening of the second stage of labor, where pushing is
contraindicated like cardiac disease, hypertensive disorders of pregnancy and previous
cesarean section
After coming head of breech
1.4. Prerequisites (for outlet and low forceps)
Well documented indication should be present
Cervix must be fully dilated
Membranes must be ruptured
Presenting part must be either vertex, mento anterior face presentation or after coming head
of breech
Head must be engaged and station should be below +2
Exact position of the head should be determined
No gross cephalopelvic disproportion (contracted pelvis or macrosomia)
Maternal bladder should be empty
Appropriate anesthesia should be given and prophylactic episiotomy done
Adequate skill and experience
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1.5. Technique of out let forceps delivery
Check the indication and the prerequisites
Put the mother in lithotomy position at the edge of the delivery coach. Clean and drape the
vulva.
Empty the bladder and insure adequate anesthesia (pudendal, local infiltration) Select the
appropriate forceps. Articulate the forceps in front of the vulva (phantoms application) in the
direction of fetal position.
Lubricate the blades with antiseptic solution
Hold the left blade with the left hand and insert 2-3 fingers of the right hand into the left side
of the vagina. Slide the left blade gently between the head and the fingers in an arc to put it
on the side of the fetal head. Initially hold it vertically then bring it to the horizontal position
through a smooth arc.
Repeat the same step for the right blade holding it in right hand and fingers of the left hand in
the vagina
Depress the handles and lock the forceps. If difficulty is encountered, remove the blades and
recheck the position of the fetal head.
After locking, check for proper application. (I. Posterior fontanel should be located midway
between the sides of the blades with lambdoid suture equal distance from the blades and
one finger breadth above the plane of the shank II. Fenestration of the blades should be
barely felt and the amount of fenestration should be equal (in solid blade no more than a
fingertip should be able to be inserted between the blade and the head). III. Sagittal suture
must be perpendicular to the plane of the shanks throughout its length.)
Apply traction along the axis of the pelvis using no more force than a force exerted by flexed
forearms. Traction should be applied gradually and sustained at its maximum intensity for not
more than 30 seconds. Then relieve for 15-20 seconds.
As head crowns make adequate episiotomy
After the head is delivered unlock and remove the forceps
Following the delivery of the placenta, inspect the lower genital tract for tear and episiotomy
for extension. Repair episiotomy and any tear.
Provide care for the neonate and check for complications on the neonate.
Document your findings
1.6. Complications of forceps delivery
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The fetal/ newborn complications are laceration of face and scalp, cephalhematoma,
subgaleal bleeding, facial nerve injury, fracture of face and skull, intra cranial bleeding and
increased risk of mother to child transmission of HIV.
The maternal complications include tears of genital tract (perineal, vaginal, and cervical),
episiotomy extension and uterine rupture with or without bladder rupture.
2. Vacuum (vantous) delivery
The vacuum extractor is a traction instrument used as an alternative to the obstetric forceps.
It is designed to deliver the fetal head by drawing the scalp into the cup forming an artificial
caput called the chignon.
The vacuum extractor has the following advantages over obstetric forceps
The vacuum cup does not take up room in the often limited space in the birth canal
The vacuum extractor brings about “autorotation” of the fetal head at the level of the pelvis
where this is best, rather than where the person using forceps choose to rotate the fetal head
Generally anesthesia is not required and the mother shares in the delivery and helps to push
Episiotomy is not always necessary
2.1. Description of the vacuum extractor
The vacuum extractor has the cup, hoses that connect the cup to the trap bottle and the
pump, trap bottle with manometer and a pump which is either manual or electrical.. There
are various types of cups made either from metals or plastics like silastic. The Malmstrom
cup is a metallic cup of three different sizes (40 mm. 50mm, 60mm) with narrow rim. It has a
hole at the center of the cup through which the chain passes. The chain passes through a
hose and gets attached to the metal cross bar. Threading the chain attaching it to the metal
bar takes some time. For these reasons the Bird's modification of the cup is developed It
has a chain permanently attached to its center on the back and a hole for the hose at the
periphery of the cup. This modification eliminates the need to thread the chain through the
hose. Later silastic cups were developed. These are soft, easy to manipulate and vacuum
is attained more quickly.
2.2. Indications
The indications are similar to forceps delivery except after coming head of breech.
2.3. Prerequisites
The prerequisites are similar to forceps but need modifications in the following.
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· Cervix need not be fully dilated. Vacuum can be applied if cervix is more than 8
centimeters dilated.
· Presenting part must be vertex
· Position need not be known
· It can be applied for higher stations. Head must be engaged station 0 or below
(descent of less than 2/5)
· Live fetus at term
· Need for anesthesia is less and routine prophylactic episiotomy is not a must
2.4. Procedure
Check the indication and the prerequisites
Put the mother in lithotomy position at the edge of the delivery coach. Clean and drape the
vulva.
Empty the bladder and insure adequate anesthesia (pudendal, local infiltration) Select the
largest cup that can easily be introduced.
Introduce the cup unto the vagina and position it over the sagittal suture about 3 centimeters
in front of the posterior fontanel.
Check the full circumference of the cup for entrapped maternal tissue
Create a vacuum of 0.6- 0.8 kg/ cm3. For silastic cups it can be done rapidly over 1 minute
where as for metallic cups gradual increment of 0.2 kg/ cm3 every 2 minutes allows adequate
caput formation.
Check again for tissue entrapment before traction.
Apply perpendicular traction using two handed technique (fingers of one hand placed at the
rim of the cup and the other hand grasps the traction bar). Sustained traction in the direction
of the pelvic curve should be applied coincident with uterine contractions and maternal
pushing.
As soon as the head is delivered release the cup and complete the delivery of the fetus and
the placenta.
Following the delivery of the placenta, inspect the lower genital tract for tear and episiotomy
for extension. Repair episiotomy and any tear.
Provide care for the neonate and check for complications on the neonate.
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Document your findings
2.5. Complications
The fetal and maternal complications are similar to forceps delivery but generally occur at
reduced incidence. Localized scalp edema which disappears in few hours, scalp abrasions
and lacerations and necrosis of scalp from prolonged application of the cup is usual.
DESTRUCTIVE DELIVERY
Destructive delivery is vaginal operative delivery that accomplishes delivery of the fetus by
reducing its size in a woman with obstructed labour with dead fetus. The advantages of
destructive delivery over caesarian section for a woman with obstructed labour and fetal
death are
The uterus will remain intact, thus avoids the risk of rupture of the uterus in the subsequent
pregnancies.
Peritoneal contamination by infected uterine contents is avoided
Risks of anesthesia and prolonged postoperative stay in bed are avoided
1. Types of destructive delivery
I. Craniotomy is destructive delivery done on the head. It involves reducing the size of the
head by removing the brain tissue through an opening made in the skull of the fetus.
Depending on the presentation the brain tissue can be approached through the suture lines
and fontanel or the palate or the foramen magnum.
II. Decapitation is destructive delivery for impacted shoulder presentation with hand
prolapse. It involves severing the neck of the fetus allowing the delivery of the rest of the
body and later the head.
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III. Evisceration is also a destructive operation for impacted shoulder presentation with hand
prolapse. It involves removing the abdominal and thoracic viscera through an opening made
in wall of the thorax or abdomen.
IV. Clediotomy is a destructive operation for shoulder dystocia. It is reduction of the
biacromial diameter by cutting the clavicles.
Note: Destructive operations should ideally be performed in an operating theatre under
general ansthesia with at least two units of cross matched blood available.
2. Prerequisites
Clear indication- obstructed labour (gross CPD, impacted shoulder presentation, shoulder
presentation)
Fully dilated cervix
Dead fetus (need to be confirmed by ultrasound or auscultation by three people
Accessible presenting part for the type of procedure selected ( head with decent of less than
2/5 for craniotomy, neck for decapitation, axilla or abdomen for evisceration)
Imminent rupture or rupture of the uterus ruled out
Access for immediate laparatomy and blood transfusion
Adequate skill and ansthesia
3. Complications
Major complications are rupture of the uterus, genital tract lacerations (perineal, vaginal and
cervical), bladder and rectal damage.
CAESARIAN SECTION (C/S)
Caesarian section is delivery of fetus or fetuses along with the placenta and membranes by
an incision made through the abdominal and uterine wall after the fetus has reached viability.
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The correct terminology for the surgical delivery of a previable fetus is hysterotomy.
Caesarian section is classified as elective (caesarian section that is performed before the
onset of labor or before the appearance of any complication that mandates an urgent
delivery) and emergency (caesarian section that is performed after the onset of labor or
appearance of a complication that mandates urgent delivery). Primary caesarian section is
one that is done for the first time while repeat caesarian section is the one that is done for
more than one time.
1. Types of caesarian section incision
I. Lower segment transverse (Kerr) caesarian section
In this type the lower segment is incised transversely after incising and reflecting the vesico
uterine fold of peritoneum. This is the most commonly done type of cesarean section and has
long been the standard operation because it has the following advantages
Less blood loss, easy to repair
Good wound healing therefore less risk of future rupture
Less risk of adhesion formation because of its peritoneal coverage.
The major disadvantages are:
Lateral extension with damage to uterine vessels and ureters
Bladder injury especially in repeat cases.
II. Classic (Sanger) caesarian section
In this type uterine incision is made vertically through the corpora uteri (upper segment). It is
simple and fast to perform but is associated with a number of disadvantages
More blood loss and difficult to close
Poor healing of the incision, therefore high chance of future rupture
Risk of adhesion formation with bowel and omentum
Therefore it is not a routine method of caesarian section and is only done upon specific
indications.
Inaccessible lower segment because of dense adhesions from previous caesarian section
Large myoma over the lower segment
Highly vascular lower segment from anterior placenta previa
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Fetal malformations like conjoined twin and transverse lie with back down
III. Less common types
Lower segment vertical (Sellheim) caesarian section
Delee incision – J-shaped extension of the lower segment transverse incision
Inverted T incision lower segment incision
2. Indications
Caesarian section is done in cases in which vaginal delivery either is not possible or would
impose undue risks to mother or baby or both. Some of the indications are clear and
absolute while others are relative. Common indications for caesarian section include
Cephalopelvic disproportion
Mal presentations (transverse lie, breech, persistent brow)
Cord presentation and prolapse
Fetal distress in the first stage of labor
Failed induction/ augmentation and instrumental delivery
Ante partum hemorrhage (placenta previa, abruption placenta)
Conditions with unripe cervix where rapid delivery is needed like preeclampsia, ecclampsia,
Previous caesarian section after failed trial of scar or electively
Carcinoma of the cervix
The X-factor relative indications, which considered separately, might not warrant caesarian
section but when taken together constitute a valid indication. Example is post term plus
elderly primigravida or prior infertility problem.
3. Procedure and patient care
Informed consent should be obtained. An intravenous line is opened and crystalloids started.
Hemtocrite and blood group should be determined. Blood should be cross matched and be
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readily available. Self or catheter assisted bladder emptying is done. Prophylactic antibiotics,
if indicated, are given. Non particulate antacids with gastric decompression by nasogastric
tube should be done in emergency cases.
Both inhalational (general) and regional (spinal, epidural) ansthesia can be used. Proper
preparation of the operative site is done.
Abdomen is opened by midline, paramedian or pfannenstein (transverse suprapubic)
incisions. The abdomen is then opened in layers. The vesicouterine fold of peritoneum is
opened transversely and bladder reflected down. The lower uterine segment is opened
transversely and the fetus extracted. The cord is clamped and cut. The placenta is delivered.
The endometrial cavity is mopped of any reminants by sterile moist pack. The edges of the
uterine incision are caught by Greenarmytage forceps. Uterine incision closed in one or two
layers by chromic 0 or 1. Hemostasis secured. Bladder peritoneum closed by continuous
chromic 2/ 0. Abdominal wall closed in layers.
Postoperatively the level of consciousness, vital signs and degree of vaginal bleeding should
be monitored frequently. Intravenous fluids are continued until the woman is taking fluids.
Do not give anything orally until bowel sound returns. Antibiotics and transfusion are given if
indicated. Encourage early ambulation.
Upon discharge ensure that she is taking regular diet, wound is clean, dry
and not infected and there is no fever. Counsel on future risks and need to
have hospital delivery in future pregnancies.
4. Complications
Complications occur during the operation or in the post operative period. Intraoperative
complications include bladder laceration especially in repeat cases, ureteral injury,
hemorrhage from damaged uterine vessels, anesthetic complications like Mendelsons
syndrome, fetal blood loss from incision through placenta or laceration at the time of incision,
trauma at time of extraction and fetal hypoxia from venacaval compression and anesthetic
drugs.
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Postoperative complications include hemorrhage from atonia or incision site, pelvic
hematoma, endomyometritis, wound site infection, deep vein thrombosis and future risk of
rupture of the scar in subsequent pregnancies. Other post operative complications seen in
any surgical patient can be encountered.
5. Vaginal birth after caesarian (VBAC)
In the absence of absolute contraindications a woman with caesarian section scar can be
given the chance to deliver vaginally. These contraindications which mandate elective
caesarian section are
Classic or inverted T or low vertical incision with extension to the corpus
Two or lower segment incisions or the type of incision is unknown
Gross CPD from macrosomia (estimated weight of more than 3500 grams) or any degree of
pelvic contracture
Multiple pregnancies
Malpresentation
Conditions that preclude vaginal delivery or need induction
Review Questions
1. List the indications of forceps and vacuum delivery.
2. List the prerequisites to forceps and vacuum delivery.
3. List the complications of forceps and vacuum delivery.
4. Name the types of destructive deliveries.
5. List the prerequisites and complications of destructive delivery.
6. Describe the major types of caesarian section with their advantages and
disadvantages.
7. List the complications of caesarian section.
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CHAPTER 17
MALPRESENTATIONS AND MALPOSITIONS
Learning Objectives
· To list the types of mal presentations and mal positions with their predisposing
factors.
· To define breech presentation and describe the varieties of breech
presentations with there diagnostic approaches.
· To describe the maternal and fetal risks associated with vaginal breech
delivery.
· To describe the techniques of conducting vaginal breech delivery.
· To know how to diagnose and manage the other mal presentations.
· To describe the options of management for persistent occipito posterior
positions.
Introduction
Malpresentation and malpositions are essentially abnormalities of fetal position, presentation,
attitude or lie. They collectively constitute the most common cause of fetal dystocia occurring
in approximately 5% of all labors.
Breech presentation is the commonest malpresentation. The other malpresentations are
face presentation, brow presentation, shoulder presentation, and compound presentation.
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The malpositions include occipito posterior position and persistent occipito transverse
positions.
Often no cause is identified but any condition that changes the proportional volume of the
fetus and amniotic fluid resulting in increased or decreased mobility of the fetus predisposes
to malpresentations. These conditions are well known and fall into three major groups.
Fetal factors: fetal anomalies like e.g. hydrocephalus, multiple gestation, prematurity,
polyhydramnios and oligohydramnios.
Maternal factors: uterine anomalies like septate and bicornuate uterus, contracted pelvis,
submucus myoma, grand multiparity and past history of malpresentations.
Placental factors: placenta previa.
1. BREECH PRESENTATION
Breech presentation is a fetal presentation where the fetus lies longitudinally and the
buttocks or the fetal lower extremities occupy the pelvic inlet with the cephalic pole occupying
the fundus.
1.1. Types and incidence
There are four types of breech presentation
Frank breech presentation: fetal with flexed hips and extended knees so that the thighs
are apposed to the abdomen and the lower legs to the chest. The presenting part is the
buttocks. It accounts for 60% - 65%of all breech presentations at term and 40% before term.
Footling breech presentation (single or double): fetus with one or both hips and knees
extended so that the feet become the presenting part. It accounts for 25%-35% of breech
presentations at term and 50%before term.
Complete breech presentation: fetus with flexed hips and knees so that the buttocks and
the feet become the presenting part. it accounts for 10% of all breech presentations at any
gestational age.
Knee presentation is a rare form seen in a fetus with extended thighs and flexed knees.
Incidence depends on the gestational age and the fetal weight. Breech presentation
accounts for 3-4% of all births but occurs in 15% of low birth weight (<2500gm) infants. Its
incidence in premature fetuses is high and decreases as gestational age increases.
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1.2. Diagnosis
There are no specific symptoms but occasional tightness or discomfort in the upper abdomen
may be reported.
Leopold’s maneuver reveals round, globular, smooth head occupying the fundus, which will
be ballotable if adequate amniotic fluid is there and narrow and softer breech occupies the
lower pole of the uterus. Fetal heartbeat will be heard more easily at or above the umbilicus.
Pelvic examination in labour identifies the soft irregular mass with anal orifice, the ischial
tuberosities, genital groove and external genitalia. In footling and complete breech
presentation one or both feet are felt.
The important differential diagnosis at this point is face presentation which should be
differentiated by the presence of the hard maxilla and if the fetus is alive the presence of
suckling.
Ultrasonography and plain film of the abdomen can be done to confirm the diagnosis.
1.3. Mechanism of labour (frank breech in left sacrotransverse position)
The denominator of breech presentation is the sacrum and the diameter is bitrochanteric
diameter. The eight possible positions are recognized: sacrum anterior (SA), sacrum
posterior (SP), left sacrum transverse (LST), right sacrum transverse (LST), left sacrum
anterior (LSA), left sacrum posterior (LSP), right sacrum anterior (RSA) and right sacrum
posterior (RSP).
In labour the breech engages as the bitrochanteric diameter passes the plane of the pelvic
inlet, usually in one of oblique diameters. Decent occurs with further flexion. Internal rotation
ordinarily takes place when breech reaches levator musculature which brings the
bitrochanteric diameter to anteroposterior position. Further decent with flexion brings the
pelvic outlet. Delivery of the buttocks, first the anterior to be followed by the posterior, occurs
by lateral flexion.
As the trunk is delivered the shoulders enter the pelvic inlet in the transverse diameter
causing rotation of the trunk so that the back faces up. The shoulders descend in the birth
canal and at the level of the pelvic floor internal rotation occur causing external rotation of the
body. At this point the back is directed to the left side of the mother, which indicates
readiness for the delivery of the shoulders. The shoulders are then delivered by lateral
flexion, anterior followed by posterior.
At the time the shoulders rotate internally the head engages in the transverse diameter of the
inlet. The head, after decent rotates internally at the pelvic floor. This causes rotation of the
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rest of the body so that the back faces up. Further decent results in the delivery of the head
by flexion (the face sweeps the perineum).
1.4. Management
I. Antepartum management
Breech presentation diagnosed before 32 weeks of gestation should be managed
expectantly with frequent follow up. Spontaneous version to cephalic presentation at
the latter weeks of gestation is likely.
After 36 weeks the chance of spontaneous version is less likely. If the there are
no contraindications external cephalic version should be performed. This requires
expertise and facilities for emergency caesarian section. If external cephalic version is
contraindicated a decision on the mode of delivery (vaginal breech delivery or elective
caesarian section) has to be made before labour starts. For these reasons pregnant
women with breech after 36 weeks have to referred for hospital management.
II. Intra partum management – vaginal breech delivery
All breech deliveries should ideally be conducted in a set up with caesarian section
facility. In the absence of such facility laboring mothers with breech presentation in
whom delivery is not imminent (cervical dilatation of less than 8 cm) should be referred.
Women in whom delivery is imminent should be attended in the same health facility. This
justifies why all health workers dealing with laboring women need to be skilled in
conducting vaginal breech delivery.
Vaginal breech delivery trial should be allowed in:
Estimated fetal weight of less than 3500gms
Frank or complete breech with flexed head
Pelvis should be judged to be adequate with favorable shape
Live fetus with normal heart rate pattern or gross malformation or dead fetus
No other obstetric factor (X factor)
Evaluation at admission is like any laboring mother (refer to). This confirms the diagnosis
and identifies parameters for allowing vaginal breech delivery. Artificial rupture of
membranes should not be done.
First stage of labor should be followed as described in chapter 14. Vaginal examination
should be done and fetal heart beat checked following spontaneous rupture of membrane to
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rule out cord prolapse. Progress of labor in breech presentation is not remarkably different
from vertex presentation. The occurrence of in coordinate uterine action, uterine inertia,
arrest or delay in cervical dilatation or failure of descent of breech warrants urgent caesarian
section. There is no place for augmentation of breech presentation with poor progress of
labour. The mother should be instructed not to push till full cervical dilatation is achieved.
In the second stage of labour, before conducting delivery, pelvic examination should be done
to confirm full cervical dilatation. Bladder must be emptied and the mothered positioned into
lithotomy position. There are three types of vaginal breech delivery.
1. Spontaneous vaginal breech delivery where the infant is expelled entirely
spontaneously with out any help other than support. This occurs rarely except for premature
babies in a multipara. It is associated with higher perinatal mortality.
2. Assisted vaginal breech delivery (Partial breech extraction) where the fetus is
delivered upto the level of the umbilicus spontaneously and the rest of the body is delivered
with the assistance of the health professional using special maneuvers.
3. Total breech extraction where the entire fetus is delivered from the birth canal by the
assistance of the health professional. It is associated with significant maternal and fetal risks.
This procedure is only performed for the delivery of the second twin.
Third stage is managed actively and the genital tract explored for tears.
III. Techniques of assisted breech delivery
A. Delivery of the buttocks and legs
Instruct the mother to bear down with every contraction. Do episiotomy when the fetal
anus is visible and perineum distended. Allow the breech to be delivered with out
intervention up to the level of the umbilicus. After the delivery of the buttocks, supporting
the baby around the hips without pulling and keeping it below the horizontal is all that is
needed. The baby should be grasped with clean towel moistened with warm water.
Holding the baby around the hips avoids fetal visceral damage. Ensure the anterior
position of the sacrum and the back until the lower border of the scapula is visible.
In frank breech, if the legs can not be delivered spontaneously, it can be assisted by
splinting the medial thigh of the fetus with the position parallel to the femur and exerting
pressure laterally so as to sweep the legs away from the midline (Pinnard maneuver).
Apply gentle and steady down word traction until the lower halves of the scapula are
delivered.
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B. Delivery of the arms and shoulders
After the lower border of the scapula is visible pull a length of umbilical cord.
Ensure the back is facing to the right or left side before delivering the arms. Introduce two
fingers into the vagina over the chest of the fetus and feel for both arms. If the arms are not
felt it indicates extended or nuchal arm. If the arms can’t be delivered spontaneously,
deliver the arms in one of the following ways:
I. Lovset maneuver
Holding the baby’s hip rotate the fetus by half a circle (1800) keeping the back
uppermost and applying downward traction at the same time. This delivers the posterior
arm, which now becomes the anterior arm, beneath the pubic arch. This may be assisted by
placing one or two fingers on the upper part of the arm flexing it, which sweeps the arm
over the chest. Then reverse the rotation (half a circle (1800) keeping the back
upper most to deliver the remaining arm beneath the symphysis.
II. Delivery of the posterior arm followed by anterior (or the reverse)
Put one or two fingers into the vagina over the back of the baby. Slip the fingers
over the shoulders, place them parallel to the humerus and apply downward pressure
to deliver the arm.
III. Extraction of the posterior arm
It is useful for extended arm and the Lovset maneuver is not successful.
C. Delivery of the head
Allow the baby to hang until the nape of the neck or posterior hairline is visible.
Then deliver the head in one of the following ways:
I. Mauriceau Smellie Veit maneuver
Introduce the non-dominant hand into the vagina over the face of the fetus which
is supported by the forearm. Place the first (index) and the third (ring) fingers on the right
and left cheek bones and place the second (middle) finger into the baby’s mouth. Pull the
jaw down to flex the head.
At the same time introduce the dominant hand into the vagina over the back of the
fetus. Put the first and third fingers over the shoulders and the middle finger over the
occipital prominence. Press down on the occiput to assist in flexion of the head.
Ask an assistant to give supra pubic pressure by the base of the hand. Pull gently
to deliver the head by making an arc following the pelvic curve.
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II. Wigand maneuver
The procedure is like Mauriceau Smellie Veit maneuvers but differs by
1. The dominant hand instead of being introduced into the vagina it is put on the
supra pubic area to provide supra pubic pressure.
2. An assistant is not needed to apply supra pubic pressure.
III. by Pipers forceps
D. Difficulties during vaginal breech delivery
I. Nuchal arms (extended arms found behind the neck of the fetus) should be
managed by Lovset maneuver or by rotating the fetus counter clock wise to deliver the
right arm and often clock wise to dislodge and deliver the left arm.
II. Extended arm is diagnosed when the arms are not felt on the chest.
Management is like the nuchal arm.
III. Arrest of the after coming head could be caused by incompletely dilated
cervix, extended head, hydrocephalus or cephalopelvic disproportion (contracted pelvis
or big baby)
1.5. Complications
Breech presentation is associated with high perinatal morbidity and mortality. Possible
complications contributing to maternal mortality and morbidity are obstructed labor, genital
tract lacerations and increased risk of operative delivery. Fetal complications are cord
prolapse, birth injury (superficial tissue damage, edema and bruising, fractures of the
humerus, clavicle or femur, dislocation of shoulder or hip, Erb’s palsy, trauma to internal
organs especially a ruptured liver or spleen, damage to adrenals, spinal cord damage or
fracture of the spine and intracranial hemorrhage) and associated congenital malformations.
2. FACE PRESENTATION
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Face presentation is a kind of cephalic presentation where the neck of the fetus is fully
extended so that the occiput lies on the back and the face (area of the fetal face between the
orbital ridges and the chin.
It is a rare condition occurring in 1 in 550 births.
2.1. Diagnosis
Antenatal diagnosis is often difficult. Diagnosis is usually made in labour by vaginal
examination. Diagnosis by Leopold maneuver is based on finding long ovoid uterus with no
bulges in the flanks, S shaped ill defined fetal back with marked depression between the
occiput and the back, and palpation of the cephalic prominence on the same side as the fetal
back. Fetal heart beat is heard on the side of the feet in mento transverse and difficult to
identify in mento posterior.
On vaginal examination, with sufficiently dilated cervix, feeling the orbital ridges, eyes, nose
and mouth clinches the diagnosis. Confusion may arise with breech presentation in
prolonged labor with edema of the presenting part. The mouth may be open and the hard
gums are diagnostic and the fetus may suck the examining finger.
2.2. Mechanism of labour
The denominator is the mentum (chin). The presenting diameter is submento- bragmatic
which is 9.5 centimeters. Eight possible positions exist depending on the relation of the chin
to the various positions of the pelvis.
Engagement occurs when the submento-bragmatic diameter passes the pelvic inlet. Decent
with extension of the head occurs. At the pelvic floor internal rotation occurs. In most rotation
of the chin occurs anteriorly so that the fetus assumes mento anterior position. In few the
chin rotates towards the sacrum assuming persistent mentoposterior position.
For mento anterior further decent with extension occurs till it reaches the perineum. Delivery
occurs by flexion so that the sinciput, vertex and the occiput sweep the perineum.
Restitution, external rotation and delivery of the shoulders by lateral flexion occur in the same
manner as vertex presentation.
For persistent mento posterior there is no further mechanism of labour. Unless relieved,
further impaction results in obstructed labour.
2.3. Management of labour
Caesarian section is indicated in the presence of big baby, contracted pelvis, previous
uterine scar like previous caesarian section and elderly primi or woman with bad obstetric
history. In labour persistent mentoposterior position, poor progress of labour and fetal
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distress are indications for caesarian section. Appropriate evaluation before or at the start of
labour and proper follow up of labour is, therefore, essential.
Follow up in the first stage of labour is like in vertex.
Labour may be slow but as long as it is progressing nothing has to be done. The old saying
"if a face is progressing leave it alone” is still valid. Augmentation of labour is generally
contraindicated.
Low forceps may be needed for mentoanterior position in prolonged second stage.
2.4. Complications
These include cord prolapse, facial bruising and swelling which disappear in one week and
1-2 days respectively, cerebral hemorrhage, extensive perineal lacerations, increased
operative delivery and obstructed labour.
3. BROW PRESENTATION
Brow presentation is a kind of cephalic presentation in which there is partial extension of the
fetal head so that the brow (area between the anterior fontanel and the orbital ridges)
becomes the presenting part.
It occurs in 0.06 % of deliveries.
3.1. Diagnosis
Diagnosis by abdominal palpation is possible but unusual. Usually diagnosis is made in late
labour. Finding the frontal suture, anterior fontanel, the orbital ridges and the base of the
nose on vaginal examination with dilated cervix clinches the diagnosis.
3.2. Mechanism of labour
The denominator is the anterior fontanel or the frontal bone. The presenting diameter is
mentovertical diameter which is 13 centimeters. Engagement does not occur as this diameter
is larger than the diameters of the pelvic inlet. Unless it reverts to either face or vertex
presentation, there is no mechanism of labour for brow presentation. Spontaneous delivery
of a term brow is unlikely. If no intervention is made the end result is obstructed labor.
3.4. Management
In the absence of other conditions that mandate caesarian section, determination of the
pelvic capacity and fetal size must be made. Emergency caesarian section is indicated for
macrosomia and contracted pelvis.
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In early labour, in the absence of such conditions, management is expectant. This is based
on the assumption that a brow may spontaneously revert to face or vertex, which occurs in
30 % of the cases. If it persists, the fetus has to be delivered by caesarian section.
Augmentation of labour for arrested labour is not recommended.
4. COMPOUND PRESENTATION
Compound presentation is a presentation in which an extremity (hand or foot) prolapses or
descends along side the presenting part. The most common type is upper extremity
prolapsing with vertex. Other varieties are upper extremity with breech or rarely lower
extremity with vertex.
Incidence is 1 in 1000 pregnancies.
Diagnosis is made on vaginal examination in labour by palpating fetal extremity adjacent to
the presenting part. If diagnosis is suspected but uncertain, ultrasound or X-ray can be used
to locate the position of the extremities and search for mal formations.
Management depends on gestational age, type of presentation and whether the hand or foot
is prolapsing. Viability of the fetus should be documented prior to delivery since compound
presentation is associated with prematurity. Labour should be allowed and delivery
anticipated, if the fetus is non-viable (<28 weeks according to our country's protocol) or has
gross congenital malformation or is dead.
For viable fetus, hand prolapsing with vertex labour could be allowed to continue with the
hope of spontaneous retraction of the hand as labour progresses. Any attempt to reduce the
extremity by digital manipulation is contraindicated. Persistent cases should under go
caesarian section.
Vertex with foot and breech with hand are indications for caesarian section.
5. SHOULDER PRESENTATION (TRANSVRESE LIE)
Shoulder presentation is a presentation in which the long axis of the fetus is at right angles to
the axis of the uterus so that the presenting part becomes the shoulder. It is the most
dangerous of the fetal presentations. Occasionally the lie is oblique but this does not persist
as the uterine contractions during labour make it longitudinal or transverse.
Incidence is 1:300 deliveries at term but is higher in preterm.
5.1. Diagnosis
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Diagnosis is easy but can be overlooked. On abdominal examination, the uterus is
transversely oval with the fundus scarcely above the umbilicus. The fundal height is less than
expected for the period of gestation. There is no fetal pole in the fundus and the pelvic inlet.
The fetus lies crosswise with head in one side of the abdomen. These findings may be
obscured after membrane rupture in late labour A very high and unreachable presenting part
on vaginal examination highly suggests transverse lie. Ultrasound confirms the diagnosis and
identifies the possible causes.
In labour vaginal examination identifies the shoulders and/ or the ribs or in neglected cases
the hand prolapsing through the vulva.
5.2. Mechanism of labour
There is no mechanism of labour for an average sized fetus. If labour is allowed to continue
obstructed labour develops.
In women with capacious pelvis and premature fetus, delivery could occur by doubling up or
spontaneous version.
5.3. Management
· If transverse lie is diagnosed antenatal, refer the patient to hospital as term
approaches.
· If shoulder presentation is diagnosed during labour, refer the patient immediately to
hospital.
· Shoulder presentation diagnosed before term should be managed expectantly since
there is a chance of spontaneous version.
· Shoulder presentation reaching term can be managed by external cephalic version.
7.6. Complications
· Cord prolapse
· Uterine rupture with possible maternal death. This is especially true in neglected
shoulder presentation.
6. UMBILICAL CORD PRESENTATION AND PROLAPSE
It is decent of the umbilical cord into the lower uterine segment. Intermittent or continuous
compression by the presenting part compromises the fetal circulation causing fetal hypoxia
and eventually death. It may take the following forms:
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Overt cord prolapse: presentation of the cord beyond the cervix after rupture of the
membranes, so that loop of cod is palpable or visible during examination.
Occult cord prolapse: with ruptured membranes the cord has prolapsed along side the
presenting part but not in front of it. This is not palpable during vaginal examination
Cord presentation: the cord is in front of the presenting part with intact membranes so that
it is felt through the membranes during vaginal examination.
Incidence varies with the type of presentation. For overt cord prolapse it is 0.5% in cephalic,
0.5% in frank breech, 5 % in complete breech, 15 % in footling breech and 20% in transverse
lie.
Any condition that provides space between the presenting part and the pelvic inlet
predisposes to cord presentation and prolapse.
Maternal factors are contracted pelvic inlet, multi parity, tumor previa
Fetal factors are malpresentation, long umbilical cord, low lying placenta, prematurity,
multiple gestation, conditions that cause rupture of membranes before engagement of the
presenting part like in PROM and polyhydraminos
Iatrogenic factors are artificial rupture membrane done for fetus at high station
Diagnosis of overt cord prolapse is done by finding loops of cord in the vagina or cervix.
Feeling loops of cord through the membrane ahead of the presenting part diagnoses cord
presentation. Diagnosis of occult cord prolapse is suspected by finding variable deceleration
following rupture of the membranes.
Management
I. Cord presentation- emergency caesarian section if the fetus is mature or is nearing
maturity.
II. Occult cord prolapse – perform pelvic examination to rule out overt prolapse. Put in a
position that corrects the fetal decelerations. If this does not correct it and the deceleration
persists deliver the fetus by the fastest route (instrumental delivery or caesarian section.
III. Overt cord prolapse – depends on presence of cord pulsation and cervical dilatation.
If there is no pulsation await spontaneous delivery with or without destructive delivery.
If pulsations are felt deliver by the fastest route (caesarian section if cervix is not fully dilated,
instrumental delivery if cephalic and cervix is fully dilated, total breech extraction if breech
and cervix is fully dilated).
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Note: If fetus is viable (FHB positive and cord pulsating) until the patient is ready for
caesarian section put the patient in knee-chest position, apply continuous up ward
pressure against presenting part , put the cord inside the vagina and give oxygen to the
mother
Complications are maternal (complications of operative deliveries) and neonatal (prognosis
depends on the degree and duration of umbilical cord compression occurring before
the diagnosis is made and neonatal resuscitation is begun. If the duration of complete cord
occlusion is less than 5 minutes, the prognosis is good).
Prevention and early detection
· Artificial rupture of membrane should be avoided until the presenting part is well
applied to the cervix.
· After spontaneous or artificial rupture of membrane, careful and prompt pelvic
examination should be done to rule out cord prolapse.
· Before doing ARM, check for the presence of cord.
7. MALPOSITIONS (VERTEX-MALPOSITION)
Occipito posterior (OP) may be normal in early labor. Most change by spontaneous rotation
to occipitoanterior position. Progress of labor is not different from that of occipitoanterior
position. But slow progress is common as the result of minor degrees of disproportion and
the long rotation of the fetal head. In 10% it persists in occipito posterior position.
Mechanism of labor in right occipito posterior position (long rotation) is the same as that of
occipito anterior position except that it undergoes long rotation. In some cases the occiput
takes short rotation to assume persistent occipitoposterior position and is delivered with face
to pubis.
Diagnosis is easily made by manual vaginal examination when one finds the posterior
fontanel directed towards the sacrum. Women may
complain of continuous and severe backache worsening with contractions.
Management of persistent occipitoposterior position is similar to that of occipitoanterior
position. One should anticipate prolonged labour from abnormal shape of the pelvis and the
long rotation of the head. In the absence of CPD, augmentation of labour is possible for
hypotonic uterine action.
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Possibilities for vaginal delivery in persistent occipitoposterior position include spontaneous
vaginal delivery with generous episiotomy, forceps delivery with or without rotation, vacuum
delivery and caesarian section for CPD.
Review questions
1. Describe the general causes of malpresentation
2. Describe the techniques used in assisted breech delivery.
3. Describe the mechanism of labour in face presentation.
4. Discuss the diagnostic features of transverse lie.
5. Describe the management of overt cord prolapse.
CHAPTER 18
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DYSTOCIA
Learning Objectives
To define dystocia and list its main causes.
To discuss the difference between hypo and hyperactive uterine dysfunction.
To list the major causes and complications of macrosomia.
To define shoulder dystocia and enumerate the steps in the management.
To discuss the clinical features and management of hydrocephalus.
To describe ideal obstetric pelvis and list the indications for pelvic assessment.
To define and classify contracted pelvis.
Dystocia is difficult labor, which is characterized by abnormally slow progress of labor. It is
the most common indication for primary caesarian section. Dystocia is a consequence of
faults in the five P’s operating alone or in combination.
· Power (uterine contraction and voluntary muscular efforts)
· Passage (bony pelvis and soft tissues of the birth canal)
· Passenger (the fetus)
· Psyche and physician
1. Faults in the power (Inefficient uterine contraction or uterine dysfunction)
Myometrial contractions in normal labor start from one of the pacemakers located in the
uterine cornu. These contractions are characterized by triple descending gradient, which
constitutes
· Propagation of contraction which is downward from the fundus to the cervix.
· Intensity of contraction that is stronger in the upper part of the uterus.
· Duration of contraction that is longer in the upper part.
· Peak of uterine contraction which occurs simultaneously in all parts.
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The net result of this is to provide effective uterine contraction, which pushes the fetus
downwards, thus dilating the cervix. In normal labor effective uterine contraction should fulfill
the following.
· Frequency of 3-4 contractions per 10 minutes
· Duration of 45-60 seconds during each contraction
· Intensity of 20-60 mm Hg with resting tone of 10-15 mm Hg (fundus of the
uterus can not be indented at the height of contraction)
Any deviation from this pattern results in uterine dysfunction. In majority of uterine
dysfunctions the cause is unknown. In the rest the following are implicated:
· Minor to moderate degrees of CPD, which result in poor application of the
presenting part to the cervix.
· Uterine overdistension as in polyhydramnios or multiple pregnancy.
· Anxiety and emotions (psychological factors), which depress release of
oxytocin from the posterior pituitary.
Uterine Dysfunction is common in primigravida than in multiparas (4% vs. 2%). It leads to
prolonged labor which intern results in maternal exhaustion, increased risk of intrapartum
and postpartum infection of the mother and fetus, fetal distress and operative deliveries.
There are two types of uterine dysfunction
a. Hypotonic uterine dysfunction (uterine inertia)
b. Hypertonic uterine dysfunction (in coordinate uterine action)
:
Hypotonic UD Hypertonic UD
Resting tone decreased Resting tone increased
Normal gradient pattern with fundal
dominance present
Distorted gradient pattern lower
segment dominance or complete
assynchronism of electrical impulses.
Contractions are decreased in intensity
with slight rise in pressure therefore,
less pain and uterus is indentable at the
height of the contraction
Contractions are increased in but are
disorganized ,therefore, contractions
more painful leading to ketosis
Responds favorably to oxytocin gets accentuated by oxytocin
2. Faults in the passenger
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The fetus may be the cause of dystocia if the presentation is abnormal, if it is big sized or if it
is grossly malformed.
I- Malpresentation
In the absence of contracted pelvis or/and big sized fetus most malpresentations and
malpositions do not cause dystocia. Significant dystocia is a rule in shoulder presentation,
persistent brow presentation, persistent mentoposterior presentation and breech with
extended head, nuchal arm and hydrocephalus.
II- Macrosomia
Macrosomia is defined as fetal weight exceeding 4000 grams. The general rule is, the larger
the size of the fetus the higher the chance of dystocia. There is no clear cut fetal weight limit
implicated in causing dystocia. In a woman with normal sized pelvis dystocia is unusual if
fetal weight is less than 3500 grams.
The causes of macrosomia are maternal diabetes mellitus especially of gestational type and
post date pregnancy. Increasing parity, increasing age and size of the mother are associated
with macrosomia.
Macrosomia should be suspected in a woman with big abdomen, fundal height of the uterus
bigger than the calculated gestational age from the LMP, fetus seems large with minimum
amount of amniotic fluid and non-engagement of fetal head at term. Fetal weight can be
estimated by Johnson’s formula and ultrasound.
Fetal weight in gram= fundal height in centimeters –n * 155
n= 12 if the vertex is above the ischial spine
n= 11 if the vertex is below the ischial spine
The anticipated complications of macrosomia are deep transverse arrest, shoulder dystocia,
post partum hemorrhage from uterine atonia or genital tract tears and obstructed labor and
its complications.
III. Shoulder dystocia
Shoulder dystocia is an acute obstetric emergency in which following the delivery of the head
the shoulders of the fetus can not be delivered despite the performance of routine obstetric
maneuvers. It results from impaction of the anterior shoulder above the symphysis pubis in
an antero- posterior diameter.
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Risk factors for shoulder dystocia, which are identified in only less than 50%, include fetal
macrosomia, maternal obesity; prolonged labor especially prolonged second stage of labor,
previous history of shoulder dystocia and difficult operative vaginal deliveries.
Diagnostic features include
· Turtle sign – following the delivery of the head the neck is retracted and the
head recoils against the perineum with the chin pressed against the maternal
thigh.
· Spontaneous restitution doesn’t occur and the face becomes plethoric.
· Failure to deliver the shoulders with maternal expulsive effort and gentle down
ward traction on the fetal head.
Complications of shoulder dystocia are post partum hemorrhage from genital tract tears and
uterine rupture, birth injuries (fractures, brachial plexus injury) and fetal asphyxia and death.
Shoulder dystocia requires prompt and skillful management. The following steps are useful.
Step1- Stop maternal expulsive efforts. Stop desperate pulling on the fetal head. Call for
help.
Step2- Disimpact the anterior shoulder by one or combination of the following
maneuvers.
· McRoberts maneuver (hyper flexion of both legs on the maternal
abdomen)
· Rubins maneuver (application of suprapubic pressure in lateral direction
on the posterior aspect of the anterior shoulder)
Step 3- Rotational maneuvers (effective anesthesia needed)
· Wood screws maneuver – rotating the posterior shoulder backward through
1800(half circle).
· Rubin rotational maneuver-Rotating the posterior shoulder forward through
1800.
Step 4- Extraction of posterior arm
Step 5- if the above fail perform symphysiotomy and clediotomy
IV- Congenital malformations
1. Hydrocephalus
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Hydrocephalus is progressive enlargement of the cranium resulting from excess
accumulation of cerebrospinal fluid in the ventricles of the brain. It accounts for 12% of
malformations at birth and occurs in 1:1000 deliveries. In one third associated defects like
spina bifida are found. Breech presentation is found in one third of cases. Significant
dystocia from gross CPD is a rule.
Clinical features, which may head in diagnosis, are broad firm mass above symphysis in
cephalic presentation and in labour finding on vaginal examination of tense large
fontanel, widened suture line and indentable thin cranial bones
Definite diagnosis requires ultrasound examination, which shows dilated ventricles. Plain
x-ray of abdomen may show large globular head with small face and thin cranial bones.
The management of diagnosed hydrocephalus is drainage of excess cerebrospinal fluid
by cephalocentesis (ventriculocentesis). This procedure involves passing long needle
through the dilated suture lines into the ventricles. It can be done vaginally (after 3-4 cm
cervical dilation in cephalic presentation or after the body and shoulders are delivered in
breech presentation) or transabdominally before the onset of labor.
2. Others
Malformations that may cause dystocia include congenital goiter and other neck
swellings, abdominal masses including ascitis, distended fetal bladder, enlargement of
liver, kidneys and spleen and conjoined twins.
Diagnosis is often difficult and should be suspected if dystocia arises after delivery of the
head .Often stillbirth is the end result.
3. Faults in the passage
3.1. Bony dystocia
The true pelvis has an inlet, mid-cavity and outlet. An ideal obstetric pelvis fulfills the
following:
· Round or transversely oval pelvic brim (inlet) without undue projection of the
sacral promontory. The inclination of the brim should be less than 550 below
the horizontal, obstetric conjugate (anteroposterior diameter) of 12 cm and
available transverse diameter of 12.5cm.
· The cavity should be shallow with straight sidewalls from which the ischial
spines do not project unduly and large sciatic notches with sacrospinous
ligament accommodating two fingers (3.5cm).
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· Outlet with rounded sub pubic angle of 850 or more (two fingers) with inter
tuberous distance of at least 10cm (4 knuckles).
CONTRACTED PELVIS results if one or more of the critical internal diameters of the
pelvis are shortened by 2cm or more. It is classified into:
I. Generally contracted pelvis-involves contracture of the inlet, midcavity and outlet.
II Inlet contracture – anteroposterior diameter of less than 10 cm OR transverse
diameter of less than 12 cm.
III. Midcavity contracture – anteroposterior diameter of less than 11.5cm or
transverse diameter of less than 9.5cm.
IV. Outlet contracture- intertuberous diameter of less than 8cm
The causes of contracted pelvis are classified as follows.
I. Normal development of the pelvic bones but with abnormal shape: android type
pelvis (triangular brim) and platypelloid type pelvis (flat oval brim which is more
common in women with short stature).
II. Nutritional deficiency from rickets (Vitamin D deficiency) in child hood and
osteomalacia in adult.
III. Diseases or injury in the spines (kyphosis, scoliosis), pelvis (pelvic tumors,
fractures) and the limbs (poliomyelitis in childhood)
IV. Congenital disorders of spines (spondtlolistesis, high assimilation pelvis), pelvis
(Naegels pelvis and Roberts’s pelvis) and the limbs (congenital dislocation of hips)
Pelvic assessment
The capacity of the pelvis can be assessed by clinical and X-ray pelvimetry. Pelvic
assessment is indicated in:
Primigravida at term with unengaged head.
Primigravida with height less than 1.5 meters or age less than 18 years.
Multipara with history of prolonged labor, stillbirth, early neonatal death or severe neonatal
injury.
Women to be induced or augmented.
Before trial of scar in lady with previous caesarian section.
Women with abnormal presentation (face, breech and brow).
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Clinical pelvic assessment should be done after emptying the bladder and putting the
woman in lithotomy position. Then one should assess the following:
Reachability of sacrum promontory. If reachable measure the diagonal conjugate.
Smoothness and concavity of sacrum.
Straightness of the sidewall and projection of the ischial spine.
Size of sub pubic angle and intertuberous distance.
Soft tissue masses and strechability of the perineum.
Management
The management of contracted pelvis depends on the degree of contracture and
presence of other obstetric complications notably malpositions, malpresentations and
macrosomia. Regardless of other obstetric complications, grossly contracted pelvis
should be managed by caesarian section preferably electively.
The management of borderline contracted pelvis depends on the presence of
other obstetric complications. Caesarian section should be done in the presence of
macrosomic fetus, malpresentation in a normal sized fetus and conditions which need
induction/ augmentation. In the absence of these a trial of labor should be given before
a decision of caesarian section.
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3.2. Soft tissue dystocia
Cause Management
A. Cervical Dystocia
Rigid cervix from stenosis digital dilation, cervical incision
Conglutination of the cervix digital dilation, cervical incision
Cervical cancer with infiltration caesarian section
B. Vagina
Septum(transverse or longitudinal) Incision or caesarian section
Incomplete atresia caesarian section
Annular stricture manual dilatation, incision or caesarian
section
Extensive scarring manual dilatation, incision or caesarian
section
Gartner duct cyst Aspirate aseptically
Tetanic contraction of levator ani anesthesia
Vulvar scar generous episiotomy
C. Pelvic masses
Myoma, ovarian cyst caesarian section
Review Questions
1. Enumerate the causes of dystocia.
2. Discuss the difference between hypotonic and hypertonic uterine dysfunction.
3. Discuss the management of shoulder dystocia.
4. Discuss the classification and causes of contracted pelvis.
5. List the indications for pelvic assessment.
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CHAPTER 19
OBSTRUCTED LABOR AND RUPTURED UTERUS
Learning Objectives
To define obstructed labor and uterine rupture.
To list the important causes of obstructed labor and uterine rupture.
To enumerate the immediate and late complications of the obstructed labor.
To discuss the clinical features obstructed labor and uterine rupture.
To outline the management of obstructed labor and uterine rupture.
To discuss the prevention of obstructed labor.
1. OBSTRUCTED LABOR
1.1. Definition-
Obstructed labor (OL) is failure of descent of the fetus in the birth canal for mechanical
reasons arising from either the passage or passenger in spite of adequate uterine
contraction. It is an absolute condition, which should be applied only when further progress is
impossible without assistance.
1.2. Importance
OL is one of the major causes of maternal mortality in developing countries. Its incidence is
mainly related to the availability, accessibility and quality of antepartum and intrapartum
services in the community and to a lesser extent to the incidence of fetopelvic disproportion
in the community. OL should never occur in communities where obstetric care is optimal
even if disproportion is prevalent. Therefore, OL is considered as a sign of major failure in
obstetric care.
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1.3. Causes
Cephalopelvic disproportion (CPD) remains to be the commonest cause of OL. Contracted
pelvis (which is prevalent in developing countries where childhood malnutrition and early
marriage are common)is responsible for most of the CPD. Macrosomic babies and fetal
malformations account for the minor proportion of CPD.
Malpresentation is the other major cause of OL. Included in here are neglected shoulder
presentation, impacted big breech, and arrested aftercoming head in breech, persistent brow
and mentoposterior presentations. In the presence of borderline contracted pelvis
mentoanterior and persistent occipitoposterior positions may cause OL.
Other rare causes of OL include deep transverse arrest, shoulder dystocia and soft tissue
obstruction.
1.4. Complications
The immediate and late complications of OL are responsible for the high maternal mortality,
stillbirth and early neonatal death associated with this condition. In those who survive
significant maternal and neonatal morbidity results in short and long term debility. The impact
of these complications is immense in developing countries where health service coverage is
low and resources are scarce.
The immediate complications include
· Atonic postpartum hemorrhage
· Uterine rupture (rare in primigravidas)
· Intra and post partum infection leading to peritonitis, sepsis and septic shock
· Maternal tetanus
· Fetal cerebral birth trauma
· Fetal distress
· Fetal and early neonatal infection and sepsis
The late complications include
· Fistulas(vesico-vaginal fistula and recto-vaginal fistula)
· Vaginal stenosis and stricture
· Foot drop(sciatic and common peroneal nerve injury)
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· Contracture of joints and ostitis pubis
· Perinatal asphyxia & mental retardation
1.5. Clinical features
Women with obstructed labour invariably give history of prolonged labor with early rupture of
membranes. Usually these women did not receive ANC during pregnancy.
On examination they are exhausted, anxious and weak. Invariably there are signs of
dehydration and intrapartum infection. In multipara three tumors abdomen is seen prior to
rupture (bladder, lower segment and thick upper segment with the Bandls ring in
between).Uterus may be hypotonic or may show strong contractions especially in multipara.
Bladder is edematous and distended with very little urine in it. Bowels are usually distended
from acidosis induced hypokalemia. Fetus may be in distress or dead. Evidence of gross
CPD (caput and significant molding) or malpresentation is found on pelvic examination.
1.6. Management
The principles in the management of OL are
· Obstruction must be relieved without delay. Before doing so, one should rectify the
effects of prolonged labor (dehydration, acidosis and intrapartum infection) partially or
fully.
· Some form of operative delivery is always needed to relieve the obstruction (vaginal
or abdominal).
· Non-operative methods like oxytocin have no place in the management of OL.
I. Resuscitation
It should be started as soon as the diagnosis is made using the available facilities and
resources. In referral cases, this has to be started at the peripheral clinic and continued
during transportation. The components are:
A .Fluid and electrolyte replacement to tackle dehydration and acidosis
· Open an intravenous line preferably with a wide bore indwelling cannula
· Infuse crystalloids fast.(for example 5%dextrose in saline with 50% glucose added )
· Monitor urine output by inserting indwelling plastic catheter (Catheterization may be
difficult if the presenting part is impacted and may require digital dislodgement .Never
use metallic catheter as this causes urethral injury.)
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B. Control infection
In all cases infection must be assumed and intravenous broad spectrum antibiotics
should be commenced prophylactically. The chosen antibiotics should cover gram positive,
gram negative and anaerobic bacteria. Initial loading dose followed by maintenance dose
should be given.
II. Preintervention preparation
· Catheterize the bladder as described above.
· Empty the stomach by nasogastric tube.
· Determine hemtocrite and blood group. Cross match at least 1 unit of blood
· Give antacids orally
III. Relief of obstruction
One should decide on the best method of delivery because it has an impact on the survival
of the mother. Unless there are contraindications vaginal route is preferred route of
delivery. The risks associated with abdominal delivery are
 Peritonitis from peritoneal contamination by infected uterine contents
 Anesthetic risks like aspiration pnumonitis
 Bladder and ureteral damage
 Bleeding from extension of the incision
 Scar on the uterus with risk of future rupture in a mother who may not return next time
Abdominal delivery (caesarian section or laparatomy for uterine rupture) is indicated in the
following conditions
 Alive fetus with incomplete cervical dilatation or preconditions for instrumental
delivery not fulfilled
 Imminent or definite uterine rupture even if the fetus is dead
 Dead fetus when criteria for destructive delivery are not met
The modes in vaginal delivery include
 Generous episiotomy if the cause is tight perineum or scarring from genital mutilation
 Vacuum is of limited value except as an adjunct to symphysiotomy
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 Forceps is limited value except in deep transverse arrest
 Symphysiotomy –limited experience
 Destructive delivery (embryotomy)
Vaginal route of delivery is contraindicated in the following conditions
 Ruptured uterus (manipulation may extend the tear or removes the tamponade
effect )
 Imminent uterine rupture (manipulation may complete the rupture)
 Alive fetus with high station or incomplete dilatation of the cervix
 Dead fetus where the criteria for embryotomy are not fulfilled
IV. Post intervention care
 Increase intake (parenteral or oral) to reverse dehydration
 Continue antibiotics (initially parenteral later oral) to complete full coarse
 Institute continuous bladder drainage by indwelling catheter for 5-7 days
1.7. Prevention
Even with aggressive management OL is associated with high mortality and morbidity both to
the mother and the fetus. Therefore, health programs should focus on prevention of OL,
which is considered to be a largely preventable condition. As a general rule, OL should never
occur in a patient who has received optimal antenatal and intrapartum care. This can be
achieved by non-sophisticated and non-expensive methods tailored to the immediate
resources of the community. Where feasible, hospital care for all is ideal.
The measures that should be undertaken to prevent OL include
 Provision of accessible family planning methods
 Provision of universal quality ANC to all pregnant women to identify risk factors
 Provision of intrapartum care (includes use of partograph) by skilled personnel who
can identify intrapartum risk factors and provide appropriate management (ranges
from early referral to provision of treatment).
 Provision of a well-organized and fully functional unit (hospital or health center) for
delivery of comprehensive emergency obstetric care. This includes availability of
functional operation theatre and blood transfusion services.
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 Provision of a good referral system for immediate transfer of mothers.
 Community education on:
· Harmful traditional practices (early marriage, female genital mutilation, harmful
maneuvers in labor).
· Importance of good nutrition in childhood and pregnancy
· Empowering women.
· Importance of ANC and supervision of labor by skilled personnel.
2. UTERINE RUPTURE
2.1. Definition and types
Ruptured uterus is defined as a tear in the wall of the uterus which commonly occurs in the
lower segment of the uterus. The tear could be anterior, posterior, lateral or combination of
these. It could be transverse, vertical or combination of these configurations. In most, it
occurs in the intrapartum period but antepartum rupture can occur especially in women with
classic caesarian section scar or scars related to other gynecologic surgeries like
myomectomy.
Rupture of the uterus is classified into two categories.
 Complete (true) - the tear extends through the whole thickness of the uterus including
the myometrium and the peritoneum so that there is free communication with the
peritoneal cavity.
 Incomplete (occult) - the tear extends through the myometrium but not through the
overlying peritoneum so that there is no free communication with the general
peritoneal cavity.
2.2. Causes
By far the commonest cause of uterine rupture is neglected obstructed labor especially in
multipara. The next common cause is rupture or dehiscence of a previous caesarian section
scar. Other causes include
 Oxytocin or prostaglandin administration
 Difficult instrumental delivery like high or mid forceps
 Difficult destructive delivery
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 Internal podalic version and breech extraction
 Difficult manual removal of placenta
 Other surgical scars on the uterus(repaired ruptured uterus, myomectomy)
 Vigorous fundal pressure and sharp penetrating trauma
2.3. Clinical features
Diagnosis of uterine rupture is usually reached using clinical symptoms and signs. But at
times it is difficult especially in those with scar on the uterus and those under regional
anesthesia. Diagnosis in these cases often needs manual exploration of the uterus and even
exploratory laparatomy.
Clinical features are variable and are largely dependant on the time elapsed after the rupture,
the site and extent of the rupture, the degree of fetal and placental extrusion(the degree of
intraperitoneal spill)and the tamponade effect offered by the fetus. Therefore, a high index of
suspicion is needed for diagnosis for those not presenting classically.
The usual symptoms of impending (imminent) uterine rupture are
 Worsening abdominal pain especially suprapubic persisting between contraction
 Strange feeling of the fetus moving upwards
The usual symptoms in uterine rupture include
 Sudden cessation of contraction and fetal movement often following a sharp tearing
pain at the height of the contraction
 Temporary relief of pain followed by diffuse, continuous abdominal pain
 Variable degree of vaginal bleeding depending on the degree of fetal impaction
 Gross hematuria in anterior wall rupture with bladder rupture
The clinical signs are also variable and include
 Normal vital signs to profound shock (tamponade effect and involved blood vessels)
 Variable pallor
 Variable abdominal tenderness and distension
 Absent uterine contraction and fetal heart beat
 In anterior rupture, defect in the uterine wall and easily palpable fetal parts
 Variable shifting dullness
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 Presenting part may be jammed or retracted with variable vaginal bleeding
Feeling a defect on vaginal examination or seeing the defect at laparatomy makes definitive
diagnosis of uterine rupture.
2.4. Management
The life of the patient depends on the speed and efficacy with which hypovolemia is
corrected, hemorrage is controlled and infection is treated. In places where surgical
intervention cannot be provided, early referral should be undertaken only after resuscitative
measures are initiated.
A. Supportive management
This has the objective of initiation of treatment for impending or full blown shock, intrapartum
infection and preparing the woman for laparatomy. Components include
· Opening intravenous line with wide bore cannula.
· Vigorous infusion of crystalloids.
· Initiation of parenteral antibiotics covering the mixed organisms like obstructed
labour.
· Performing laboratory tests for hemoglobin and blood group/RH status.
· Preparing at least two units of cross matched blood.
· Inserting naso-gastric tube and folley catheter.
B. Definitive management
Immediate laparatomy should be performed .The surgical options include
· total abdominal hysterectomy
· sub- total abdominal hysterectomy
· repair of the rupture with bilateral tubal ligation
Review Questions
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1. Define obstructed labor and list the important causes.
2. Describe the complications of obstructed labor.
3. Discuss the management and prevention of obstructed labor.
4. Discuss the clinical features and management of ruptured uterus.
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CHAPTER 20
FETAL DISTRESS
Learning Objectives
To define fetal distress and describe its pathophysiologic basis
To list the etiology of fetal distress with emphasis to iatrogenic causes
To discuss the diagnostic features of fetal distress
To describe the management of fetal distress
Fetal Distress is the sign of inability to withstand the stress of labor leading to asphyxia,
which if prolonged, places the fetus at risk of permanent neurologic injury, multiple organ
failure and eventually death .There is no single indicator that definitely diagnoses fetal
distress but abnormal fetal heart rate patterns and fetal scalp PH determination (where
available) are usually used in the diagnosis.
1. Pathophysiology
A normally grown fetus has stored reserves of glycogen and fat to be used at times of stress
like labor. In labor temporary cessation of placental transfer of oxygen and nutrients occur
during uterine contraction. This results in anaerobic metabolism with accumulation of lactic
acid and carbon dioxide that increases as labor progresses. This is normally corrected
between each contraction provided there is adequate oxygen carrying capacity of the
mother, adequate perfusion of the placenta, adequate relaxation period between
contractions (resting tonus), good umbilical blood flow (patent vessels) and adequate fetal
energy reserve.
Failure to correct this mild form from pathological conditions results in progressive
accumulation of lactic acid and carbon dioxide. This results in acidosis and reduction of
oxygen ending up in asphyxia .The net effect is change in fetal heart beat, which forms the
basis fir diagnosis and in extreme cases passage of muconium.
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2. Etiology
In general all forms of fetal distress originate from deficient delivery of oxygen to the fetus.
Some occur as the result of sudden catastrophic events like massive abruptio placenta and
cord prolapse. Some are iatrogenic in origin.
I. Uterine and placental factors
 Increased tone and frequency of contraction from oxytocin induction and
augmentation and precipitate labor
 Decreased placental surface area from abruptio placenta
 Uteroplacental insufficiency from post term pregnancy and hypertensive disorders of
pregnancy
II. Umbilical cord
 Cord prolapse either iatrogenic or spontaneous
 Cord compression from oligohydramnios and entanglement and knot
III. Fetal factors
 Limited or exhausted reserve like in intrauterine growth restriction, prolonged labor
and fetal anemia (example isoimmunization)
IV. Maternal factors
 Decreased oxygenation from cardiac and respiratory diseases, severe anemia,
smoking
 Decreased blood pressure from sudden maternal shock (example APH), supine
hypotension syndrome and conduction anesthesia
3. Diagnosis
The diagnosis of FD is usually based on
I. Abnormal fetal heart rate patterns
An abnormal FHR pattern is associated with high false positive rate; therefore, it should be
used as a screening method for which additional methods (scalp PH) are needed for
confirmation. In the absence of confirmatory tests combination of abnormal patterns should
be used to increase the sensitivity. .The abnormal patterns include
 Baseline bradycardia is classified as moderate (fetal heart beat of 80-100/min for >3
min) and severe (fetal heart beat of <80 /min for > 3 min)
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 Baseline tachycardia is classified as mild (fetal heart beat of 161-180 /min for >15
min) and severe (fetal heart beat of > 180 / min for > 15 min)
 Repeated late deceleration
 Severe recurrent variable deceleration (drop of FHB to < 70/ min with duration of > 60
sec)
 Reduced beat to beat variability
II. Fetal scalp blood PH and gas analysis
Currently, it is the best method to assess the acid base status of the fetus. It needs special
gas analyzer and is not available in all settings.
4. Management
The management of fetal distress has two components
I. Correction of the potential insults (intrauterine resuscitation)
 Put the mother in left lateral position
 Start intravenous infusion of fluids(dextrose in saline with 40 %glucose)
 Give oxygen by mask at the rate of 8-10 liters/minute
 Discontinue oxytocin
 Correction of hypotension of regional anesthesia
 For cord prolapse put in knee chest position and disimpact the presenting part
 Others- amnioinfusion for cord compression
-acute tocolysis with terbutaline till delivery
II. Remove the fetus from the hostile environment
Deliver the fetus by the most expeditious route. This is accomplished by caesarian section (if
in the first stage or if prerequisites for instrumental delivery are not met in the second stage)
or by instrumental delivery (if in the second stage).
Review questions
1. Describe the pathophysiology of fetal distress.
2. Enumerate the causes of fetal distress.
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3. Discuss the management of fetal distress.
References
1. DeCherney AH, Pernoll ML Current. Obstetrics and Gynecologic diagnosis and
treatment, 8th edition, 1994.
2. Lawson J. B, Stewart D. B, Obstetrics and Gynecology in the Tropics and developing
countries
3. Scott JR., DiSaia PJ, Hammond CB, Spellacy WN: Danforth’s obstetrics and Gynecology,
8th edition, 1999.
4. Novak’s text of Obstetrics & Gynecology, 10th edition, 1981.
5. Addis Ababa University faculty of medicine department of Obstetrics and Gynecology:
Guideline for management of obstetric and gynecologic problems, 1st edition, 2003.
6. Bennett V.Ruth and Brown Linda K.: MYLES text book for mid wives, 13th edition
7. Llewellyn Jones D, Fundamentals of Obstetrics and Gynecology, Volume 1, Fifth edition,
1990
8. Kenneth R. Niswander, Manual of Obstetrics, diagnosis and therapy, 1st edtion, 1982
9. John Cook, Surgery at district hospital, Obstetrics and Gynecology 1991
10. Dreissen F, Obstetric problems, A practical manual, 1991
11. WHO, Department of reproductive health and research, integrated management of
pregnancy and childbirth. Managing complications in pregnancy and childbirth. A guide for
midwives and doctors, 8.
12. MOH/ FHD, Technical Guidelines in managing maternal and new born care
13 Cunningham F. Gary et. al, Williams Obstetrics,20th edition, 1993
14. King M, Bews P, Karins , Thornton J: Primary surgery, Volume 1 (Non trauma); Oxford
medical publication, 1990
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PART IV
NORMAL AND ABNORMAL
PEURPERIUM
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CHAPTER 21
NORMAL PUERPERIUM AND ITS MANAGEMENT
Learning objectives
· To describe the normal changes of puerperium
· To know the conduct of normal puerperium
· To detect and manage abnormal puerperium
Introduction:
Puerperium is the period of adjustment following pregnancy and delivery when anatomic
and physiologic changes of pregnancy are reversed and the body returns to non pregnant
state. This period of adjustment traditionally extends to six weeks postpartum. It is classified
into three phases
· Immediate extends from delivery to 24 hours postpartum
· Early extends from 24 hours to the end of the first week
· Late extends from the end of the first week to complete involution of the generative
organs which is traditionally 6 weeks
Physiologic changes of puerperium
1. Involution
This is a process by which the reproductive organs return to the pre-gravid state.
The uterus from a size of 20 weeks (at or just below the umbilicus) just after delivery reduces
in size at a rate of one finger per day. By the end of the first week it is 12 weeks, by 10 -14
days it becomes impalpable per abdomen and reaches non gravid state by 6 weeks. Its
weight reduces from 1000 grams at the end of delivery to 50- 100 grams by 6 weeks.
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In the first 2- 3 days after delivery the uterus contracts strongly causing lower abdominal
discomfort and pain. This is called the after pain and is commonly seen in multiparas. It is
worse after suckling.
The endometrium, besides the placental site, differentiates into superficial and basal layers in
2-3 days. The superficial layer gets necrotic and is cast off as lochia. Regeneration of the
basal layer is completed in 10- 16 days. The placental site is reduced by 50% following
delivery. Regeneration starts by day 7 and is completed between 3-6 weeks.
Lochia is an alkaline discharge of variable amount from the uterus during puerperium.
Depending on the color, it is classified as
· Lochia rubra reddish discharge from day 1- 4 which rapidly becomes reddish brown
and mainly contain blood.
· Lochia serosa pink colored discharge from day 5-9
· Lochia Alba thick yellowish whitish discharge starting from day 10 and extends for
variable period. It mainly contains white blood cells and degenerated decidual cells
The cervix becomes a little more than one centimeter dilated at the end of the first week, and
then closes slowly. For those that have delivered vaginally, the external os changes to
transverse slit. Complete healing and re epithialization of laceration takes 6-12 weeks.
Vagina, perineum and abdominal wall regain their tone but some degree of laxity remains.
The torn hymen forms carenculae myrtiformis. Traumatic lesions of the vagina and the vulva
heal in 5-7 days.
2. Systemic changes
Enlargement of the kidneys persist for moths. Glomerular filtration rate returns to normal in 8
weeks. Ureteric dilatation persists for 12 weeks. Urinary ladder capacity is increased with
little increase in intravesical pressure. Incomplete emptying results in more residual urine.
Diuresis of the excess extra cellular fluid starts between days2-5 and causes weight loss of 4
kilograms.
There is rapid consumption of clotting factors in the first few hours after delivery. But after the
first day, there is rapid crease in clotting factors which reaches maximum y days 3- 5 and
maintained for 2 weeks.
Leukocytosis of upto 25000 per mm3 is common.
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Blood volume returns to normal in third week. Blood pressure tends to increase is the first 5
days owing to the increase in peripheral resistance. Cardiac output takes moths to return to
normal.
3. Endocrine changes
Most protein placental hormones, like human placental lactogen, become undetectable within
one day. HCG levels gradually decline and disappear by 11-16 days. Estrogen and
progesterone levels also decline to reach their lowest between 3-7 days.
The pitutary gland, which has increased in size by 30- 100% during pregnancy, starts to
regress after the first week. In non lactating mother, prolactin level returns to non pregnant
level by 2 weeks. In lactating mother, it remains above the non pregnant level with dramatic
increase during suckling. Depending o the frequency of feeding, this response gradually
declines over a period of 6- 12 months.
With the disappearance of human placental lactogen, relative hyperinsulinemia develops
resulting in lower fasting ad postprandial glucose levels. In diabetic women insulin
requirements fall.
4. Return of fertility and menustration
Follicular phase level of estrogen is reached in 19- 21 days in non lactating, in 60 – 80 days
in lactating and menstruating women vagina up to 180 days lactating amenorrhic women.
FSH ad LH levels are very low in the first 10- 12 days in all women Levels then reach
follicular phase levels at the end of second and third weeks.
Menustration resumes in six weeks in 30% and in 12 weeks in 70% of non lactating women.
In lactating women the range for resumption of menustration is 2-18 months, with 70 %
starting to have ovulation by 36 weeks.
In non lactating women, ovulation resumes as early as 33 days. In lactating women this is
highly variable and is largely dependent on the strength of suckling (frequency and duration
of each feeding and weaning). The earliest time of ovulation in lactating women is 10 weeks,
with only 20 % ovulating in six months.
5. Initiation and maintenance of lactation
Two events needed for the initiation of lactation are drop in placental hormones mainly
progesterone and estrogen and release of oxytocin and prolactin by suckling reflex (letdown
reflex). This reflex is a neuroendocrine reflex. The first milk (colostrum) has high fat and
antibody content with little casein.
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Advantages of breast feeding includes acceleration of uterine involution, provides postpartum
contraception, provides nutrients and antibodies to the neonate, it is ideal food at right
temperature and is sterile, does not need preparation and enhances mother to child bonding.
Risks are mother to child transmission of HIV in HIV positive mother, development of cracked
nipples and mastitis.
Lactation suppression can be achieved by tight fitting brassiere, giving estrogen alone or
combined with testosterone and bromocryptine.
Conduct of normal puerperium (Post partum care)
Depending on the practices in different settings, women with uncomplicated labour and
delivery can be discharged in 6 to 24 hours. Adequate patient support at home is essential.
· Adequate rest during the day and a good night sleep is essential. Insomnia, which is
a common during early puerperium, should be treated with sedatives.
· Early ambulation as of the second day. This will accelerate involution, helps in
drainage of lochia, and reduces deep vein thrombosis and constipation. Usual
household activities should be started after three weeks including postpartum
exercises.
· The importance of nourishing diet with high calorie and high fluid intake should be
stressed.
· Bathing can be take as soon as the woman is ambulatory. Vaginal douching should
be avoided in early puerperium. Perineal hygiene using clean soap and water should
be do e twice a day. Perineal pads are used as needed and should be properly
disposed.
· Encourage periodic voluntary micturition every four hours to prevent acute urinary
retention.
· Sexual intercourse may resume when bright bleeding ceases, the vulvar lacerations
have healed and the woman is physically comfortable and emotionally ready.
Physical readiness usually takes three weeks.
· Care of the baby which includes breast feeding, immunization, weaning practice and
hygiene.
· Breast care
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· Contraception: Risks of pregnancy with or without breast feeding should e discussed.
Family planning methods should be started as early as possible (2-3 weeks)
depending on free informed choice of the mother. Abstinence till the postpartum visit
is one option. Natural methods can be used in highly motivated couples. But it
needs the resumption of normal menstrual cycle. Barrier methods such as condoms
and spermicidals can be used except the cervical cup and diaphragm. Hormonal
contraceptives mainly progesterone only pills, injectables and implants can be used
safely. Intrauterine device can be inserted after 6 weeks. Permanent methods of
contraception mainly tubal ligation can be done immediately (within 72 hours) or after
6 weeks.
· Danger symptoms that include persistent bloody lochia, offensive lochia, severe
perineal pain or swelling, fever, unilateral painful swelling of the legs and playful
swollen breast.
· Provision of medications: analgesics for afterpain and perineal pain, sedatives for
insomnia, sitz bath for episiotomy and perineal lacerations, hemathenics for anemia,
anti D gamma globulin for RH negative unsensitized women with RH positive
neonate, antibiotics if indicated
· Postnatal follow up: It is usually conducted after 6 weeks.
Review questions
1. Define puerperium.
2. Describe the physiologic changes of puerperium.
3. Discuss the management of normal puerperium.
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CHAPTER 22
POSTPARTUM HEMORRHAGE (PPH)
Learning objectives
· To define PPH and describe the important causes of PPH
· To identify high risk factors for PPH.
· To outline the management of PPH. .
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· To describe the techniques of manual removal of placenta.
· To describe the diagnosis and management of uterine inversion.
Introduction
Postpartum hemorrhage (PPH) accounts for 25% of direct maternal deaths and affects 5.8%
of vaginal deliveries. PPH is a description of an event not a diagnosis; therefore, one should
identify the cause before giving specific treatment. It is the second commonest cause of
maternal death in Ethiopia. In developed countries, better obstetric care and use of oxytocic
drugs has reduced the incidence of primary PPH from over 15% to fewer than 4% of all
deliveries.
1. Definition and classification
Post partum hemorrhage is defined as blood loss of more than 500ml following vaginal
delivery of the fetus and 1000 ml following delivery of the fetus by caesarian section or a fall
in hemtocrite of more than 10% from predelivery values or bleeding following delivery
causing change in the vital signs. Depending on when it occurs, it is classified into three.
Third stage hemorrhage is PPH that occurs between the delivery of the fetus and the
delivery of the placenta.
Primary PPH is PPH that occurs within the first 24 hours of the delivery of the fetus.
Secondary PPH is PPH that occurs between 24 hours of the delivery of the fetus and 6
weeks postpartum.
2. Primary PPH
2.1. Causes and predisposing factors
There are four major causes of primary PPH.
I. Uterine atonia
This account for 50% of primary PPH. Predisposing factors include
· Over distended uterus from multiple pregnancy, polyhydramnios and macrosomia.
· Exhausted or weak myometrium from prolonged/obstructed labor, chorioamnionitis,
induction/augmentation of labor using oxytocin, anesthesia with halothane, precipitate
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labour and conditions which decrease nutrient supply to the uterus ( anemia and
hypotension of any cause).
· Previous history of uterine atony
· Others; - full bladder, grandmultiparity (more than five children), uterine liomyoma and
APH (ante partum hemorrhage from placenta previa and abruptio placenta).
II. Genital tract trauma (lacerations)
This causes 20% of primary PPH and includes bleeding from perineal tears, episiotomy
extensions, vaginal tears, cervical tears and ruptured uterus. It also includes pelvic
hematoma. The risk factors are precipitate labour, difficult instrumental and destructive
deliveries, macrosomia, shoulder dystocia, caesarian section and difficult manual removal of
the placenta.
III. Retained placenta cotyledons and membrane
This mainly results from the mismanagement of the third stage of labour (controlled cord
traction before the signs of separation of the placenta and failure to properly examine the
placenta following its delivery).
IV. Coagulation and bleeding disorders
The risk factors include severe preeclampsia/ ecclampsia, severe abruptio placenta,
prolonged intrauterine fetal death, amniotic fluid embolism, anticoagulant treatment and
bleeding disorder before pregnancy.
2.2. Management
Call for help! Effective management of primary PPH requires team work. One group is
involved in resuscitation and at the same time another group has the task of
identifying and treating the cause of the bleeding.
I. Resuscitation
Establish an intravenous line. Take blood for hemoglobin, blood group and Rh factor
determination and cross matching.
Start infusing intravenous fluids fast. Rate depends on the extent of bleeding and vital sign
derangement.
Insert an indwelling bladder catheter and record urine output.
Take vital signs frequently.
II. Identify the cause and institute appropriate treatment.
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Step1. First assess the tone of the uterus per abdomen .If the uterus is firmly contracted;
uterine atony is unlikely and proceed to step 2. If the uterus is flabby and soft institute the
following management for uterine atony.
Make sure that the bladder is empty.
Initiate uterine contraction by either rubbing up the uterus and by giving oxytocic drugs like
pitocin or ergometrine or prostaglandins. Oxytocin can be given as an infusion of 20 I.U. in
1000 ml dextrose in saline initially run fast until the uterus contracts well then at the rate of
40 drops/min. The dose of ergometrine is 0.25 – 0.5mg intramuscular or intravenous which
can be repeated every 5 minutes to maximum of 1.25 mg. Hypertension and cardiac
diseases are a relative contraindication for ergometrine use. It may inhibit subsequent uterine
exploration because of titanic uterine contraction. If no intravenous access oxytocin 10 IU
intramuscular or intramyometrial can be given.
If bleeding continues despite the above measures one should perform bimanual
compression of the uterus. This is a life saving obstetric procedure which must be
performed by all health professionals attending deliveries. The first part of the procedure
involves grasping the posterior aspect of uterine fundus and pushing it down to the
symphysis by the nondominant hand per abdomen. The second part of the procedure
involves inserting sterile gloved other hand into the vagina and placing the first and second
fingers on either side of the cervix in the anterior fornix and push it up and anteriorly. Then
massage the uterus with both hands while compression of the uterus is maintained. The
pressure should be applied continuously for 5 minutes.
If the bleeding continues surgical intervention should be taken without delay. The options
range from conservative surgery of uterine or internal iliac artery ligation to radical surgery of
hysterectomy (subtotal or total). Manual compression of the aorta can be done while
preparing for surgery or during referrals. This method can be kept for hours.
Step2. Inspect of the perineum, the vagina and the cervix under good light for laceration
or tears. Inspection of the vagina is done with the help of vaginal specula and all the walls
are inspected. Inspection of the cervix requires placement of two oval forceps on the lips
of the cervix which are rotated alternatively to cover the whole circumference of the
cervix.
Management of genital tears is repair of the tears.
Step3. If no tear is found then perform manual exploration of the uterus under aseptic
conditions for reminants of the placenta and to detect uterine rupture.
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For reminants the management is manual curettage or postpartum curettage by manual
vacuum aspiration or postpartum curret, which must be done under the cover of oxytocin.
For uterine rupture laparatomy must be done.
Step4. If no reminants or uterine rupture is found on manual exploration then consider
coagulopathy as a cause of primary PPH.
The management is treating the underlying cause and replacing clotting factors by fresh
whole blood or fresh frozen plasma.
2.3. Prevention
The most important preventive measure for uterine atony is universal application of active
third stage management. Prevention of risk factors during ANC (like anemia) and intrapartum
period (like prolonged labour) is also equally important.
Provision of controlled delivery of the fetus and adhering to the principles of instrumental and
other operative deliveries reduces genital tract trauma.
Proper third stage management prevents PPH from reminants.
3. Secondary PPH
3.1. Causes
Retained placental pieces or blood clot or membrane
Sub involution of the uterus
Endomyometritis
Undiagnosed genital tract tear
Uncommon: Necrotic fibroid, choriocarcinoma, chronic inversion
3.2. Management
I. General
a. Treatment of shock
b. Start antibiotics
c. Investigations- hemoglobin, white blood cell count, ultrasound for reminants, HCG
in titer and others
II. Specific
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a. Evacuate the uterus under oxytocin. oral ergometrine may be continued for 3-5
days.
b. Sitting or semi-sitting position assists in gravitational drainage.
c. Treat anemia
d. Rarely hysterectomy and exploration may be required.
3.3. Prevention
Proper examination of the placenta and membranes.
Clean delivery.
Prophylactic antibiotics when there are any of the predisposing factors.
4. Retained Placenta
Retained placenta is the term used when the placenta is retained with no part of it extracted
or delivered after 30 minutes of the delivery of the fetus. Retained placenta causes third
stage hemorrhage and if this does not occur it predisposes to puerperal sepsis.
The possible causes are uterine inertia, constriction ring, retracted cervix, pathological
adherence of the placenta (placenta accreta) and mismanagement of third stage.
The management of retained placenta is removal of the placenta. Before removal is
attempted, an intravenous line should be opened and blood for hemtocrite, blood grouping
and cross matching should be taken.
To determine the method of removal of the placenta, first assess the size and tone of the
uterus abdominally and perform vaginal examination to assess the degree of cervical
dilatation and the presence of placental tissue in the cervix or vagina. Depending on the
degree of placental separation and cervical dilatation the retained placenta can be delivered
by one of the following methods.
· Controlled cord traction as described in chapter
· Manual removal of placenta
· Postpartum curette in pieces
Manual removal of the placenta is a basic life saving obstetric procedure. It is indicated in
third stage hemorrhage, retained placenta of more than 1 hour and in active third stage
management when the cord is severed or if the placenta is not delivered by controlled cord
traction in 5 minutes.
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The potential complications are cervical tear, uterine rupture, PPH secondary to remnants of
the placenta and puerperal sepsis.
Technique
Manual removal has to be done after catheterizing the bladder and opening an intravenous
line. Some sort of analgesia/ ansthesia has to be used like pethidine 25-50mg and diazepam
10-20 mg intravenous or ketamine. Lithotomy position is adopted. Remove the placenta as
follows,
The vulva and protruding cord are cleaned with antiseptic solution.
Controlled cord traction is tried for last time.
Stop oxytocin drip just before manual removal to allow the cervix to relax, so that the fingers
pass through it.
Hold the cord with the left hand. The right hand traces the course of the umbilical cord
through the vagina and cervix into the uterus to palpate the edges of the placenta.
Identify the physiologic line of separation by gentle pressure using the ulnar border of the
hand. Failure to identify this line suggests adherent placenta and further attempt to separate
the placenta should be abandoned at once.
Once the physiologic line of separation is identified, gently separate the placenta from the
wall of the uterus with a slow sawing movement with the ulnar border of your hand. After full
separation of the placenta, remove it by holding it in the palm of the hands. Inspect the
placenta for completeness. Reintroduce the hand to explore the uterus for any pieces that
may have been left behind and for intactness of the uterus.
Following successful removal, give ergometrine 0.25 – 0.5 mg intravenous or intramuscular
and continue oxytocin drip. Assess the tone of the uterus. Inspect the lower genital tract for
tears. Give prophylactic antibiotics. Monitor the vital signs and observe for vaginal bleeding.
5. Uterine inversion
Uterine inversion is the prolapse of the fundus to or through the cervix so that the uterus is in
effect turned inside out. It could be incomplete (fundus is inverted but does not protrude
through the cervix) or complete (the fundus has prolapsed through the cervix and may even
be visible at the vulva)
Depending on the duration it is classified into three.
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Acute inversion is that occurs immediately after delivery or within 24 hours post delivery
(before the cervix retracts).
Sub acute inversion is that occurs between 24 hours and before 4 weeks after delivery (the
cervix already retracted).
Chronic inversion is that occurs after 4 weeks following delivery.
Acute uterine inversion
Acute uterine inversion is an acute obstetric emergency which occurs 1 in 2000-2500
deliveries. The exact etiology is unknown. For acute inversion to occur the following
conditions must be fulfilled.
The cervix must be dilated,
The placenta must be fundally attached,
The fundus must be relaxed (from congenital weakness or prolonged labour or magnesium
sulphate induced) and
A force pushing down the fundus (strong traction on the cord before placental separation
without controlled cord traction or vigorous fundal pressure)
The predisposing factors are mismanagement of third stage (pulling on the cord before
separation and failure to do controlled cord traction), fundal pressure in a relaxed uterus like
Crede maneuver, adherent placenta, vigorous manual removal of placenta and previous
history of uterine inversion.
Clinical features
The patient typically presents with severe or dull aching pain in the lower abdomen (from
stretching of the ovaries). Vaginal bleeding is variable and largely depends on the degree of
placental separation.
Shock, which is out of proportion of the degree of vaginal bleeding, in the third stage or soon
after should arouse the possibility of acute uterine inversion (mainly of neurogenic origin).
Failure to palpate the uterus and feeling of cup like depression instead on abdominal
palpation and feeling of the fundus as a dark red-blue mass in the vagina or the cervix on
vaginal examination confirms the diagnosis. The placenta may or may not be attached.
Prevention
· Proper third stage management (wait for signs of placental separation before cord
traction and apply counter pressure).
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· Avoid excessive traction on the cord
· Avoid excessive fundal pressure.
· Avoid excessively vigorous manual removal of the placenta.
Management
Resuscitation which includes aggressive and prompt treatment of shock by two intravenous
lines (crystalloids and later blood are used).
Specific treatment is immediate replacement of the uterus by manual repositioning of the
uterus. Where available, hydrostatic repositioning of the uterus can be done. If these fail
immediate referral for surgical repositioning of the uterus must be done.
Review Questions
1. Describe the causes and predisposing factors of primary PPH.
2. Describe the management of primary PPH.
3. Describe the techniques of the following life saving procedures.
A. Bimanual compression of the uterus
B. Manual removal of placenta
C. Inspection of the cervix and repair of cervical tear
4. Describe the diagnostic features and the management of acute uterine inversion
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CHAPTER 23
POSTPARTAL COMPLICATIONS
Learning Objectives:
To define puerperal sepsis and list the predisposing factors
To describe the causes and the management of puerperal sepsis
To describe the clinical characteristics and management of breast engorgement and acute
mastitis
To list the clinical features of deep vein thrombosis
To describe the psychosocial complications that can occur during post partum period.
1. PUERPERAL SEPSIS
1. Definition and etiology
Puerperal sepsis is a temperature elevation of 380c (100.40F) or more occurring at least twice
after the first 24 hours and before the tenth postpartum day and ascribed to genital origin. It
is a general term which describes any infection of the genital tract after delivery.
WHO defines it as infection of the genital tract occurring at any time between the onset of
rupture of membranes or labour and 42nd postpartum day in which 2 or more of the following
are present: pelvic pain, oral temperature of 38.50c or more at any one occasion, abnormal
vaginal discharge or pus, delay in involution of the uterus (<2 cm/day) and abnormal odor of
the discharge.
In majority, it is an ascending infection caused by the normal polymicrobial flora of the vagina
and the gastrointestinal tract. These include aerobes, facultative anaerobes and anaerobes
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of both gram positive and gram negative types. Rarely exogenous microorganisms may
cause puerperal sepsis like Clostridial and Staphylococcal infections. This occurs by using
contaminated instruments and hands or by inserting foreign objects into the vagina.
2. Incidence and risk factors
It is one of the most common complications of puerperium occurring in 1-3 % o vaginal
deliveries and 25- 50 % of caesarian deliveries. It is still a significant cause of maternal
deaths in developing countries.
The risk factors could be local or systemic. They include
Route of delivery- the single and most important actor (risk is 5-8 times higher after
caesarian section as compared to vaginal delivery)
Prolonged rupture of membranes of > 12 hours
Prolonged labour of > 12 hours
Multiple pelvic examinations
Chorioamnionitis
Intrauterine manipulations like manual removal of placenta
Reminants of placenta and genital lacerations
Systemic factors like immunosuppressive conditions (diabetes and HIV/AIDS), anemia,
Use of prophylactic antibiotics
3. Differential diagnosis
The following extragenital infections may cause fever in the postpartum period. These
must be ruled out by history, physical examination and appropriate investigations. These
conditions are urinary tract infection (cystitis and pyelonephritis mainly caused by E. coli),
acute mastitis, breast engorgement, thrombophlebitis, acute febrile illnesses (malaria,
relapsing fever and others) and other less common causes of fever like pneumonia.
4. Types of puerperal sepsis
4.1. Endomyometritis
It is infection of the endometrium and myometrium. It is the commonest form of puerperal
sepsis. It usually starts from the placental site and adjacent endomyometrium. If
untreated it progresses to pelvic cellulitis, pelvic peritonitis and generalized peritonitis,
pelvic abscess, septicemia/ septic shock and pelvic thrombophlebitis.
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Symptoms are fever o variable degree which often starts on the 3rd post partum day,
profuse and malodorous lochia (absent in Group B streptococcal infection), lower
abdominal pain initially central and later on as the disease progresses may involve the
lower quadrants and the rest o the abdomen and constitutional symptoms like malaise.
The physical findings are temperature of >38.80c, tachycardia, tachypnea in advanced
cases, lower abdominal tenderness and uterine tenderness with sub involution. Signs of
pelvic and generalized peritonitis indicate complicated endomyometritis. Evidence of
septic shock may be found.
Laboratory investigations reveal leukocytosis with let shift and positive blood culture in
some cases.
Complications include pelvic peritonitis and generalized peritonitis, pelvic abscess, pelvic
thrombophlebitis, septic shock and as late complication infertility and ectopic pregnancy.
Management, therefore, should be aggressive. All cases should be admitted.
Specific measure is initiating multiple broad spectrum parenteral antibiotics covering the
causative organisms (gram positives, gram negatives and anaerobes) and continued until the
patient is fever free for 24- 48 hours. In our setting the antibiotic regimen uses ampicillin, an
aminoglycoside and metronidazole. If reminants is suspected or diagnosed evacuation of the
uterus under the cover of oxytocin infusion should be done.
General measures like resuscitation with intravenous fluids; maintenance of electrolytes and
bowel decompression if paralytic ileus occurs, antipyretics and bed rest in the semi- fowler
position should be started. Monitoring for progress can be done by measuring the vital signs
four times a day, performing abdominal examination daily and checking white cell count on
daily basis.
NOTE. If fever is still present 72 hours after initiation of treatment or if the
condition of the patient worsens or if abdominal tenderness increases reevaluate
the patient and revise the diagnosis (consider peritonitis, pelvic abscess, pelvic
thrombophlebitis, other febrile illnesses and drug resistance).
Prevention is by following aseptic technique during labor, avoiding traumatic delivery,
avoiding repeated pelvic examinations, preventing prolonged labour by using partograph,
using prophylactic antibiotics when needed, proper third stage management to prevent
remnant and treating systemic illnesses and nutritional deficiency.
4.2. Wound infections
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It includes episiotomy site infections, infections of lower genital tract tears, and abdominal
wound infections after caesarian section or laparatomy.
Episiotomy site infection presents with persistent pain and offensive discharge from the site.
Fever is variable. Finding a tender, indurated, swollen and reddened wound edges with or
with out discharge clinches the diagnosis.
Signs of abdominal wound infection include persistent pain over the wound and tender,
indurated, swollen, and reddened wound edges. Fever with no apparent cause which
persists to the fifth postoperative day should arouse suspicion of postoperative wound
infection.
Management is removal of sutures and drain abscess if any and provision of local wound
care with antiseptic solutions. Antibiotics indicated only if there are systemic signs of
infections. Secondary closure may be needed after signs of infection have cleared.
2. BREAST COMPLICATIONS
1. Breast engorgement
It results from lymphatic and venous congestion (not from over distension of the breast with
milk). It often occurs within 48 hours of delivery. Most often both breasts are swollen, tender,
tense, and warm. Temperature may be mildly elevated but doesn’t exceed 380c.
Management includes expression of milk by hand or with a pump or by breast feeding the
neonate. If sever and persistent suppression of lactation may be needed. Supporting the
breast with a binder or brassiere and applying cold compress to the breast helps.
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2. Acute postpartum mastitis
It is an infections condition of the breast caused by staphylococcus aureus. It usually
presents near the end of the first week post partum and often involves one of the breasts
(unilateral). If not treated it may end up in breast abscess. Presenting complaints include
fever, chills, and painful swelling of the breast. Patient has tachycardia with temperature of
greater than 380c. The involved breast is hot, tender and swollen. In case of abscess
formation there will be tender fluctuant mass.
Management is cloxacillin 500 mg orally every six hours for 7 days, antipyretics and support
of breast with bra and cold compress. Breast feeding can be continued. If abscess is
diagnosed it must be drained.
2. DEEP VEIN THROMBOSIS (DVT)
Pregnant women are at increased risk of DVT because of hypercoagulable state o the blood
and prolonged immobilization that commonly occurs in the immediate postpartum period. It is
an emergency condition that should be treated promptly and aggressively.
Symptoms are painful swelling of one of the legs (rarely bilateral) which is occasionally
associated with fever.
Signs are swollen and tender thighs and calves positive ‘Homan’s sign’ (pain on dorsiflexion
of the foot).
The feared complication is pulmonary thromboembolism and subsequent death.
Management includes immobilization o the leg and immediate referral of the patient to a
setting where anticoagulant therapy can be initiated and monitored.
3. PSYCHOSOCIAL COMPLICATIONS
Three different types of postpartum psychosocial disorders have been described.
1. Postpartum blues
It is characterized by mild mood disturbances, marked by emotional instability (crying spells
apparently with no cause, insomnia, exaggerated cheerfulness, anxiety, tension, headache,
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irritability, etc). Usually the complaints develop with in the first postpartum week and continue
for several hours to a maximum of ten days and then disappear spontaneously.
The management is for one of the medical or nursing staff to talk with the women,
explaining what is occurring, and restricting visitors.
2. Postpartum depression
It is a more protracted depressive mood with complaints of affective nature; the woman is
gloomy, depressed, irritable, sad, insomniac, anorexic, poor concentration, and loss of libido.
The management is support and encouragement, psychotherapy and use of
antidepressants.
3. Puerperal psychosis
Symptoms usually start at the end of the first week, sometimes in the second week, seldom
later and tend to recur in the next pregnancy. The woman is anxious, restless, and
sometimes manic with paranoid thoughts or delusions. She reacts abnormally towards her
family members.
Management includes psychotherapy, antipsychotic treatment and isolation of the neonate
from the mother.
Review Questions
1. Define puerperal sepsis.
2. List the risk factors for puerperal sepsis.
3. Describe the complications and the management o endomyometritis.
4. List the risk factors for DVT.
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References
1. DeCherney AH, Pernoll ML Current. Obstetrics and Gynecologic diagnosis and
treatment, 8th edition, 1994.
2. Lawson J. B, Stewart D. B, Obstetrics and Gynecology in the Tropics and developing
countries
3. Scott JR., DiSaia PJ, Hammond CB, Spellacy WN: Danforth’s obstetrics and Gynecology,
8th edition, 1999.
4. Novak’s text of Obstetrics & Gynecology, 10th edition, 1981.
5. Addis Ababa University faculty of medicine department of Obstetrics and Gynecology:
Guideline for management of obstetric and gynecologic problems, 1st edition, 2003.
6. Bennett V.Ruth and Brown Linda K.: MYLES text book for mid wives, 13th edition
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PART V
GYNECOLOGY
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CHAPTER 24
THE MENSTRUAL CYCLE AND ITS ABNORMALITIES
Learning Objective:
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· To characterize the normal menstrual cycle including the phases of endometrial and
ovarian cycle
· To know the changes observed during climacteric.
· To know the clinical importance of menstrual cycle
· To describe the different abnormalities of menustration
· To discuss the approach in the management of abnormalities of menustration
A. THE MENUSTRAL CYCLE
1. Introduction
There are periodic physiologic changes in women in reproductive age group. For these
changes to occur there should be a well controlled coordination between hypothalamus,
pituitary, ovary and end organs to result in menstruation. Cessation of these physiologic
changes after reproductive age results in atrophy of reproductive organs, vasomotor
symptoms and other health hazards.
Menustration is orderly, periodic sloughing of progestational endometrium accompanied by
blood. The first menses is called menarche and the last one is called menopause.
Characteristics of normal menstrual cycle are:
· Duration of flow is on average 5 days( range1-8 days)
· Average cycle length is 28 days (range 21 to 35 days)
· Amount of flow on average is 30 ml (range10-80ml)
· Menustral blood is dark red and non clotting
2. Hypothalamo pitutary ovarian cycle
At the beginning of each cycle the hypothalamus secretes increasing amount of GNRH
which in turn stimulate the anterior pitutary to secrete increasing amount of FSH
(increases from basal level of 5-20 MIU/ml at the beginning of the cycle to reach peak of
12-30 MIU/ml at mid cycle). LH secretion in early part of the cycle also increases but at a
much lower level.
FSH stimulates the growth of a cohort of primary follicles in the ovary out of which only
one becomes the dominant follicle (Graffian follicle). As the follicles grow increasing
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amount of estrogen is produced. Estrogen exerts negative feedback effect on the
hypothalamus and pitutary, mainly on the secretion of FSH.
At around midcycle there is a surge in the production of estrogen (from basal level of 20-
60 pg/ml to more than 200pg/ml at the surge) which positive feedbacks the hypothalamus
and the pitutary. As the result, there is an increased production of gonadotrophins, mainly
LH (the LH surge- from basal level of 5-25 MIU/L to peak of 25-100 MIU/L).
LH finalizes the maturation of the Graffian follicle, which is culminated by ovulation some
24 hours after the surge. Under the effect of LH it is changed into corpus luteum. The
corpus luteum starts secreting increasing levels of progesterone (from follicular phase of
less than 2 ng/ml to luteal phase levels of 2-20 ng/ml) and to a lesser extent estrogen.
Because of the increasing negative feedback, levels of FSH and LH decline. Starting day
20 the corpus luteum regresses and eventually dies. Estrogen and progesterone
production declines, thus, lifting the negative feedback on the hypothalamus. Increased
secretion of GNRH then starts another cycle.
In summary, the ovarian cycle has three phases that are of clinical importance. These
are:
I. Follicular phase (estrogenic phase) which is of variable length
II. Ovulation transient period which occurs at mid cycle
III. Luteal phase (progestational phase) which is always 14 days in length.
3. Endometrial cycle
Because of the systemic effects of estrogen and progesterone, the endometrium
undergoes histologic cyclic changes that culminate in menustration. There are three
phases in this cycle.
I. Menustral phase starts from day 1 and usually lasts 3 to 5 days. During this phase
there is irregular sloughing of the superficial two thirds of endometrium (decidua
functionalis) accompanied by blood. This combination forms a coagulum in the
endometrial cavity, which under normal circumstances undergoes lysis before expulsion
from the uterus. Expulsion is aided by uterine contraction.
II. Proliferative phase starts near the end of the menustral phase. During this phase the
basal layer of the endometrium (decidua basalis), under the influence of estrogen,
proliferates to regenerate the superficial layer that is shaded during menses. This
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involves both the stromal cells and the endometrial glands. Histologically, the glands are
straight without secretory activity and the stromal cells are compact.
III. Secretory phase extends from ovulation to the onset of the next menustration. During
this phase the proliferative endometrium, under the influence of progesterone, is changed
to secretory type. Glands become tortuous and exhibit secretory activity. Stromal cells
are separated by interstitial edema. These changes are maximal between days 20 to 22,
after which regressive changes are seen in preparation for menses.
4. Mechanism of menustration
In the absence of pregnancy, decreasing levels of progesterone from the dying corpus
luteum, result in dehydration of the stroma. As the result there is increased coiling of the
spiral arteries, which supply the superficial layer of the endometrium. There is also spasm
of these arteries. The resulting ischemia from these mechanisms is followed by necrosis
and sloughing of the superficial layer in haphazard manner, which is shaded as
menustration. Prostaglandins initiate uterine contraction.
B. ABNORMALTIES OF MENSTRUATION
1. Abnormal uterine bleeding (AUB)
This is defined as bleeding from the female genital tract that is abnormal in amount,
duration, frequency or any combination of these.
1.1. Patterns of AUB
· Polymenorrhea is menses occurring regularly at interval of less than 21 days
(frequent menses)
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· Oligomenorrhea is menses occurring regularly at intervals of more than 35 days
· Hypermenorrhea (menorrhagia) is excessive bleeding during a menses with regular
intervals. This could occur within the normal flow time or may manifest as prolonged
flow time.
· Hypomenorrhea is unusually small menustral bleeding during a menses with regular
intervals.
· Metrorrhagia (intermenustral bleeding) is bleeding occurring at any time between
menstrual cycles.
· Menometrorrhagia is uterine bleeding, usually excessive and prolonged, occurring
at irregular, frequent intervals
· Contact bleeding: (Post coital bleeding): is self – explanatory but must be
considered a sign of cervical cancer until proved otherwise.
1.2. Causes of AUB
Depending on the age of the patient one or more of the following clinical conditions could be
cause AUB.
Early pregnancy complications like abortion, ectopic pregnancy and hydatidiform mole are
the commonest causes of AUB in women during reproductive age.
Genital tract infections like vaginitis, cervicitis, endometritis and rarely salphigo oophoritis
could be causes of AUB in sexually active women.
Tumor conditions of the genital tract (anatomic causes) are usual causes of AUB in
women nearing menopause. Malignant tumors often cause AUB in perimenopausal and
postmenopausal women. Tumors arise from any part of the genital tract but with differing
prevalence.
· Uterine: endometrial polyp, endometrial hyperplasia, liomyoma, adenomyosis,
endometrial cancer and sarcoma of the uterus.
· Cervix: ectropion, erosion, cervical polyp, cervical cancer
· Vagina and vulva: varicosities, condylomas, cancerous conditions (rare)
· Fallopian tube: rare
· Ovaries: functional cysts, polycystic ovaries, endometriosis, benign and malignant
tumors
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Systemic diseases: endocrine disorders (thyroid, adrenal, anterior pitutary), liver and renal
diseases, bleeding disorders, hypothalamic diseases like anorexia nervosa
Medication related: hormonal contraceptives, intrauterine contraceptive devices,
anticoagulant treatment
Trauma related: sexual intercourse, foreign bodies
Extragenital causes: urinary tract (hemorrhagic cystitis) and anal canal (hemorrhoids,
fissure) lesions are not actually causes of AUB, but should be ruled out to avoid wrong
diagnosis
Dysfunctional uterine Bleeding is a diagnosis by exclusion
1.3. Approach to a woman with AUB
Appropriate history and physical examination as described in chapter 2 supplemented by
necessary laboratory investigation will identify the cause of AUB.
In the history, emphasis should be given to the age of the patient, parity, the last menustral
period (LMP), duration and extent of the complaint (amount and length of menstrual flow,
cycle interval, intermenustral bleeding, if sexually active post coital bleeding and associated
pain), age at menarche and where applicable age at menopause, vaginal discharge history,
multiple sexual partners and history of sexually transmitted infections, past and present
medical illness and medication, urinary and rectal symptoms
Physical examination should focus on vital signs and signs of anemia, secondary sexual
characteristics, abdominal and inguinal masses, thorough pelvic examination (inspection of
the vagina, vulva and cervix, digital palpation for the size, consistency and surface of the
cervix and uterus, Palpation of the adnexa and pouch for mass). In addition signs for
endocrine and other medical illnesses should be looked for.
Depending on the findings appropriate investigations should be ordered. These include
complete blood count, serum or urine for HCG, cytologic examination (Pap smear),
pathologic examination of endometrium after endometrial biopsy or curettage using manual
vacuum aspiration or dilatation and curettage, ultrasonography, hysterosalpingography,
fractional curettage (curettage of the endocervix followed by dilatation of the cervix and
curettage of the endometrium) and others.
1.4. Management of AUB
This depends on the specific etiology of AUB. Refer to the different chapters that deal with
each cause.
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2. Dysfunctional uterine bleeding (DUB)
Exclusion of pathologic causes of abnormal bleeding establishes the diagnosis of
dysfunctional uterine bleeding. Virtually, all variations of DUB can be related to disruption in
normal ovarian function. Greater than 80% of DUB is anovulatory and the remaining 20% is
due to dysfunction of corpus luteum or endometrial abnormalities.
DUB most commonly occurs at the extremes of reproductive age (20% of cases occur in
adolescence and 40% in patients over age 40).
2.1. Pathophysiology
In anovulatory conditions there is continued estrogen stimulation of the endometrium. There
are two mechanisms of bleeding. One is estrogen breakthrough bleeding where the
endometrium outgrows its blood supply and will desquamate in an irregular manner. The
other is estrogen withdrawal bleeding where the endometrium sheds when the estrogen
levels decline sharply. The pattern of bleeding is dependent entirely on the duration and level
of estrogen stimulation and may take any pattern of AUB. Characteristically, anovulatory
DUB is acyclic, unpredictable as to the onset of bleeding, and variable in the duration and
amount of bleeding.
Ovulatory DUB is usually associated with premenstrual symptoms such as breast
tenderness, dysmenorrhea and weight gain, and regular periodicity. It is a result of the
dysfunction of the corpus luteum which in most cases has short life span.
Abnormalities in endometrial physiology involving chemicals like prostaglandins may be a
cause of DUB.
Uterine bleeding secondary to such pathologic entities as blood dyscrasia,
endocrinopathies, hepatic dysfunction, and other iatrogenic causes with no organic
pathologic factors should not be considered as true DUB but rather as pseudo DUB.
2.2. Diagnosis
DUB is a diagnosis by exclusion (organic causes of AUB should be ruled out
before diagnosis of DUB is entertained).
2.3. Treatment
Individualized treatment plan should be designed according to the patient age,
the desire for contraception or fertility and the severity and chronicity of the
bleeding.
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The goals of treatment should be arresting the acute episode of bleeding, preventing
recurrences and inducing ovulation if patient desires to conceive.
In adolescents pregnancy related complications should be ruled out first. Acute bleeding
episode with vital sign derangement should be treated with intravenous fluid resuscitation.
Bleeding can be arrested either by dilatation and curettage or suction curettage or
administration of high dose estrogen followed by medroxy progesterone acetate.
Recurrences can be prevented by 3-6 months coarse of combined oral contraceptives or
intramuscular progesterone in oil.
Hysterectomy is rarely needed for this group of women.
In women in reproductive age group (20-40 years) pregnancy related complications and
organic lesions should be ruled out. Management of acute episode and prevention of
recurrences is as for adolescents. In addition ovulation induction can be given for those
anovulating women who desire pregnancy. For persistent cases hysterectomy can be offered
provided that the woman has no desire for future pregnancy.
In Perimenopausal women appropriate work up must be done to rule out neoplastic
conditions including Pap smear and endometrial sampling. Management includes hormonal
treatment using progesterone derivatives or combined oral contraceptives or surgical
treatment using dilatation and curettage or hysterectomy.
3. Premenstrual Syndrome (PMS)
This is a psychoneuroendocrine disorder with biologic, psychologic and social
manifestations. It occurs cyclically prior to menstruation and then regress or disappears
during or after menstruation.
3. 1. Epidemiology
Premenstrual symptoms have been described to occur in 15% to 100% of women of
reproductive age, with 5% to 10% reporting severe symptoms at some point in their lives.
The highest incidence is in the late twenties to early thirties. PMS is rarely encountered in
adolescents and there is an intercultural variability of the type of premenstrual complaint.
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3.2. Etiology and pathophysiology
A single cause for PMS has not been identified. Multiple factors have been proposed of
which hormonal hypothesis is widely favored. The other presumed theories include; fluid
retention theory, hypoglycemia hypothesis, prostaglandin and psychologic theories.
Mittlschmerz (periovulatory ovarian pain), premenstrual molmina, bloating, breast soreness
and menstrual cramps are symptoms that usually accompany normal menustral cycle. When
these symptoms are severe, the premenstrual syndrome (PMS) and dysmenorrhea result.
They occur in the first 7 to 10 days prior to menstruation. During these days, women are
more likely than usual to absent themselves from work, to require hospital admission,
involved in accidents, to commit crimes, to develop acute psychiatric symptoms and to
commit suicide.
3.3. Clinical Features
The common symptoms associated with premenstrual syndrome include:
Affective symptoms: sadness, anxiety, anger, irritability, labile mood
Cognitive symptoms: decreased concentration, feelings of isolation and withdrawal,
indecision, paranoia, suicidal ideation
Pain: headache, breast tenderness, joint and muscle pain
Neurovegetative: insomnia, hypersomnia, libido change
Autonomic: nausea, palpitations, alteration in bowel habits
Central nervous system: clumsiness, dizziness
Fluid / Electrolyte: weight gain, edema
Dermatologic: acne, dry hair
Behavioral: decreased motivation, poor impulse control, craving for salt and sugar
PMS is usually considered significant if the severity of the symptoms interferes with day to
day activity of the woman. This general definition serves to differentiate premenstrual
molmina from the more severe symptoms characteristic of PMS.
3.4. Diagnosis
It relies on a patient’s self reporting of symptoms that she feels increase significantly during
the premenstrual period and diminish following menses.
A careful history and physical examination are most important to exclude organic causes
localized to the reproductive, urinary or gastrointestinal tracts.
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3.5. Treatment alternatives for PMS
There is no specific treatment for PMS but a number of treatment modalities have been tried.
A. Non pharmacologic modalities like modification of exercise, nutrition and stress.
B. Pharmacologic modalities, which are empiric and controversial, include ovulation
suppression (GNRH agonists, danazol, combined oral contraceptives and progestins) and
anxiolytics/ antidepressants.
C. Surgical modality (bilateral oophorectomy) is rarely needed.
.
4. Dysmenorrhea
This signifies painful menustration which prevents normal activity and requires medication.
There are two types of dysmenorrhea, primary and secondary.
4.1. Primary Dysmenorrhea
This is a type of dysmenorrhea in which no organic pelvic pathology can be found. Primary
dysmenorrhea generally begins with the onset of ovulatory cycles, typically six months to 1
year after the onset of menarche.
Incidence varies from population to population.
Symptoms include a colicky abdominal pain localized to the mid line or lower quadrants, with
radiation often noted to the lower back and legs. The pain usually starts twenty four hours
before the onset of menses, and may extend for 24 to 36 hours after the onset of bleeding.
Accompanying symptoms may include nausea, vomiting, headaches, anxiety, fatigue,
diarrhea, syncope and abdominal bloating.
Diagnosis is by exclusion of organic pelvic pathologies causing secondary dysmenorrhea.
Treatment options include
A. Prostaglandin synthesis inhibitors (non steroidal anti-inflammatory drugs).
Reported success rate ranges from 70 – 80 %.
B. Ovulation suppression by hormones like combined oral contraceptives.
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C. Calcium channel antagonists (verapamil and nifedipine)
D. Surgical treatment like presacral neurectomy, uterosacral transection can be
done for those who did not respond to medical therapy.
4.2. Secondary dysmenorrhea
Dysmenorrhea that occurs in association with organic pelvic pathology is termed as
secondary dysmenorrhea.
Causes include endometriosis, uterine liomyoma, and intrauterine contraceptive devices
(IUCD), pelvic adhesions secondary to chronic pelvic inflammatory disease and pelvic
surgery, cervical stenosis, imperforate hymen and transverse vaginal septum.
Secondary dysmenorrhea is unusual before the age of 25. The pain is not limited to the
menses. It is less related to the first day of flow and may be associated with other symptoms
like dysparunia, infertility and abnormal bleeding.
Management is directed against the specific cause.
5. Amenorrhea
5.1. Definition and classification
Amenorrhea is defined as the absence of menstruation at any time between the usual ages
of puberty and menopause. It is classified as
Primary amenorrhea: is the absence of spontaneous menses by age 16
regardless of the presence of secondary sexual characteristics or absence of
both by age 14.
Secondary amenorrhea: is the absence of menses for more than or equal to 6
months in a woman with regular cycles or for a period of more than three cycle
length in women with irregular cycle.
5.2. Causes of amenorrhea
I. Physiological amenorrhea results from pregnancy, lactation, prior or directly after
menarche and after menopause. It accounts for 90-95 % of amenorrhea. Pregnancy is the
commonest cause of physiologic amenorrhea.
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II. Pathologic amenorrhea results from pathologic conditions affecting the hypothalamus,
pitutary, ovaries, uterus and the outflow tract. It accounts for 5-10 % of amenorrhea.
Depending on the level of gonadotrophins, it is subdivided into hypogonagotrophic,
hypergonadotrophic and eugonadotrophic amenorrhea.
Hypogonagotrophic amenorrhea
Hypothalamic causes are the most common causes of this type amenorrhea. It is usually a
diagnosis by exclusion. Stress (physical, psychological), acute weight loss, anorexia nervosa
and strenuous exercise are functional causes of hypothalamic amenorrhea. Drugs like
psychotropic drugs, drug addiction and post pill amenorrhea operate at this level. In Kallman
syndrome, a rare condition there is congenital absence of GnRH along with anosmia.
Pituitary causes include hyperprolactinemia (amenorrhea-galactorrhea syndrome) either drug
induced or from prolactinomas, damage to the pitutary (trauma, surgery and irradiation),
postpartum ischemic necrosis of the anterior pitutary (Sheeans syndrome) and destruction by
craniopharyngioma.
Hypergonadotrophic amenorrhea
This results from congenital (primary) or acquired (secondary) ovarian failure.
Primary ovarian failure is seen in pure gonadal dysgenesis, Turner’s syndrome (45, X0), and
testicular regression syndrome, resistant ovary syndrome and enzyme deficiency.
Secondary ovarian failure, also called premature ovarian failure (amenorrhea before 35
years of age), results from surgery, radiation, chemotherapy, autoimmune diseases, pubertal
mumps, and genetic predisposition.
Eugonadotrophic amenorrhea
Uterovaginal causes include congenital absence or acquired destruction of the endometrium
as seen in Mullerian agenesis, Testicular feminization syndrome, isolated atresia of the
uterus, Ashermans syndrome, radiation atrophy, granulomatous infections like tuberculosis
and post hysterectomy.
Conditions that are associated with obstruction to outflow of menustral blood are cervical and
vaginal atresia, transverse vaginal septum and imperforate hymen.
Other causes are mild hypothalamic dysfunction, hyperandrogenism (polycystic ovary
disease, androgen producing ovarian tumors, adrenal tumors, Cushing’s syndrome and
congenital adrenal hyperplasia) and systemic diseases (hypothyroidism, hyperthyroidism,
and chronic renal failure).
5.3. Importance
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Amenorrhea is important for several reasons:
Failure to ovulate causes infertility.
Prolonged estrogen deficiency results in health hazards
Amenorrhea with some estrogen production can predispose to endometrial cancer.
Primary amenorrhea in a girl who has not already developed secondary sexual
characteristics may give rise to major social and psycho sexual problems.
It may be a sign of other pathologies.
5.4. Diagnosis
In majority of the cases diagnosis is reached by history, physical examination and simple
laboratory investigations. The rest need sophisticated and expensive investigations.
I. History
Points to be included in the history are:
For physiologic causes – age, pregnancy symptoms, lactation
For central causes - life style, general health condition, abnormality with smell
and vision, nipple discharge, headache, seizure, vomiting, head injury,
medication history, history of PPH, weight changes,
For ovarian causes - hot flushes, history of surgery, chemotherapy and
surgery, pubertal mumps, family history
For outflow causes – cyclic lower abdominal pain, history of curettage,
symptoms of tuberculosis, sexual difficulty, abdominal surgery
For hyperandrogenism – pattern of hair distribution, voice changes, body habitus
change, breast changes
For medical illnesses – renal disease, symptoms of hypo and hyperthyroidism
II. Physical examination
It must assess
General - body build, stature, obesity, height and weight
HEENT - eyes, hirsutism, temporal recession of hair
Glands – lymphadenopathy, breasts (Tanner staging,
galactorrhea), thyroid for enlargement, inguinal mass
Abdomen - striae, lower abdominal and flank mass
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Vaginal examination –clitoral enlargement, vagina (patency, if not patent for
bluish membrane at the vulva or septum in the vagina or blind pouch), cervix
(presence, texture), uterus (presence, size), adenexa (masses)
Rectal examination if vagina is not patent
Intgumentary system – hair distribution
Central nervous system – visual field examination
III. Investigations
Pregnancy must be ruled out by urine or serum HCG determination. Depending on the
type of amenorrhea and the clinical findings the following investigations can be ordered
Hormone assays: prolactin, LH, FSH, thyroid hormones,
Ultrasound, skull X-ray and other imaging techniques
Buccal smear for sex chromatin and chromosomal analysis
Laparatomy/ laparoscopy
5.5. Work up of Secondary amenorrhea
I. Rule out pregnancy by history, physical examination and urine HCG.
II. Perform progestin challenge test like medroxy progesterone acetate 10mg daily for 05
days.
Presence of withdrawal bleeding (positive test) after 2-7 days signifies normal estrogen
primed endometrium, normal outflow tract and absence of endogenous progesterone
(anovulation).
Absence of withdrawal bleeding (negative test) signifies absence of estrogen primed
endometrium which may result from either faults in the hypothalamus/ pitutary/ ovary/ or
endometrium/outflow tract. Further test is needed to differentiate these.
III. Perform combined estrogen- progesterone challenge test by giving drugs like
combined oral contraceptives.
Presence of withdrawal bleeding (positive test) indicates absence of endogenous estrogen
and progesterone arising either from ovarian failure or hypothalamo pitutary failure. To
differentiate these, determine LH/ FSH levels. Low FSH/LH levels diagnose hypothalamo
pitutary failure. High levels diagnose ovarian failure.
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Absence of withdrawal bleeding (negative test) indicates either obliteration of the
endometrium by synechia (Ashermans syndrome) or destruction/atrophy of
endometrium. To differentiate these hysterosalpingography is needed.
5.6. Work up of primary amenorrhea
I. Check for secondary sexual characteristics
II. If secondary sexual characteristics of feminizing type are present, check the vagina and
for pelvic mass.
If there is bluish membrane which bulges with straining and associated pelvic mass –
Imperforate hymen
If there is a blind ending vagina with pelvic mass – transverse vaginal septum
If vaginal canal does not exist and there is pelvic mass – isolated vaginal agenesis
Normal vagina with absent cervical os and associated pelvic mass – cervical atresia
If there is a blind ending vagina without pelvic mass, two possibilities exist which can be
differentiated by Barr body determination. These are testicular feminization syndrome
(Barr body negative and presence of inguinal mass) and Mullerian agenesis (Barr body
positive).
III. If secondary sexual characteristics of virilizing type are present
Consider mild form of congenital adrenal hyperplasia, post pubertal adrenal hyperplasia and
virilizing adrenal/ ovarian tumors.
IV. If secondary sexual characteristics are absent with infantile but normal sexual organs
If height is less than 147 cm consider Turner syndrome (XO) and panhypopitutarism. Check
for other features of these conditions.
If height is greater than 147 cm consider true gonadal dysgenesis (XX or XY) or Kallman
syndrome. Refer for karyotyping and LH/FSH levels.
It could be an idiopathic delay
5.7. Management
The management principles of amenorrhea are:
I. Treatment of the underlying pathologic entity
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Hyperprolactinemia- Bromocryptine and or surgery/ radiation
Craniopharyngioma – surgery
Ovarian tumor – surgery followed by hormone replacement
Systemic diseases – treatment of the underlying systemic disorder
Autoimmune oophoritis – corticosteroids
Stress – life style modification (change)
Anorexia nervosa - psychotherapy
2. Treatment of the medical needs of the amenorrhic patient
Ovulation induction or assisted reproductive technology for infertile couple
Estrogen replacement for primary amenorrhea (Reduce risk of osteoporosis,
cardiovascular complications and genital atrophy)
Cyclic progesterone treatment for those with unopposed estrogen action
Plastic surgery or vaginal dilators for blind vagina
Gonadectomy for those with dysgenetic Y gonads and undesended testis.
Psychotherapy
Review questions
1. Discuss the menustral cycle.
2. Describe the patterns of abnormal uterine bleeding.
3. Discuss the causes and the management of primary dysmenorrhea.
4. Describe the work up of secondary amenorrhea.
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CHAPTER 25
CLIMACTERIC AND RELATED PROBLEMS
Learning objectives
To define climacteric and menopause
To describe the physiologic changes of climacteric
To discuss the health problems of climacteric
To enumerate the causes of postmenopausal bleeding
Definitions
Climacteric is the phase of life for women that marks transition from being able to reproduce
to being non-reproductive. Menopause is cessation of physiologic uterine bleeding (the last
menustration). It is diagnosed retrospectively. It is the most visible event marking climacteric.
The average age at menopause is 51 years and is not affected by race, number of
pregnancies, contraceptive use, age at menarche and physical characteristics. In practice
these two terms are used interchangeably. Pre-menopause is the period before menopause
during which the menstrual cycle is irregular and climacteric symptoms are experienced.
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Post menopause is the period after menopause. Perimenopause includes the
premenopause and postmenopause and extends from 40-55 years.
Pathophysiology
As menopause nears, ovarian follicles get depleted and become resistant to gonadotrophic
hormones. Estradiol production diminishes which inturn results in elevated FSH and later LH
levels. Oligoovulation or anovulation results in menustral irregularity and unopposed
estrogen action on the endometrium. Later there will not be any follicles to be stimulated by
high levels of gonadotrophins resulting in significant drop in estrogen to a level that is not
capable of stimulating the endometrium causing menopause. The hypoestrogenic state that
follows menopause results in a number of medical conditions associated with climacteric.
Changes in menopause
I. Hormonal changes
Change in FSH and LH levels is the most striking hormonal change of climacteric. Both
exceed 40 IU/liter and continue to rise for 2-3 years and thereafter remain stable or slightly
decrease. FSH levels are higher than LH levels for the first time in the woman’s life.
Changes in estrogen levels are the last hormonal change in climacteric. Estradiol levels
become very low and levels of < 20pg /liter is diagnostic of climacteric. The predominant
estrogen in climacteric is estrone, a result of peripheral conversion of androgens.
Progesterone levels are very low in climacteric.
Levels of androgens like dehydroepiandrosterone sulfate, androstendione and testosterone
fall.
II. Reproductive organs
Effect depends on the level of endogenous estrogen. In typical hypoestrogenic states of
climacteric atrophic changes occur.
Atrophy of the vagina results in thinning of the epithelium and flattening of the rugae which
gives it the appearance of smooth, shiny pale surface.
Atrophy of the cervix reduces its size creating shallow fornices. Vaginal dryness results from
decreased cervical mucus production.
Uterus decreases in size from reduction in myometrial thickness. The endometrium
atrophies.
The ovaries reduce in size and are impalpable.
Supporting structures and muscles lose their tone.
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The labia lose fat and flatten.
III. Menustral cycle
Changes in menustral cycle are the first clinical evidence of climacteric. The usual pattern is
gradual increase in cycle length and reduction in amount and duration of flow. Heavy
bleeding and abrupt cessation are unusual.
IV. Other organs
Bladder and urethral epithelium atrophy
Breasts decrease in size
Generalized thinning and loss of elasticity of the skin results in wrinkling that is prominent on
light exposed areas (face, neck and hands).
Accentuated bone loss
Problems of climacteric
These are related mainly to estrogen deficiency and rarely to estrogen excess.
Problems of estrogen deficiency
Hot flush is the most common and characteristic subjective symptom of climacteric. It is an
episodic vasomotor disturbance consisting of sudden flushing (feeling of heat or burning in
the face, neck and chest) immediately followed by outbreak of sweating affecting the whole
body. It is seen in 75% of women in climacteric. In 25-50% it may persist for more than 5
years. In severe cases it may come as frequently as 1-2 hours. These women suffer from
insomnia. For severe cases treatment with estrogens or progestins is recommended.
Osteoporosis is the most important health hazard of climacteric. It affects the trabecular
bone. It may end up in pathologic fracture of the spines and the other bones. Diagnosis
needs special imaging investigations. Treatment is estrogen replacement. It is prevented by
estrogen replacement.
Atherosclerotic disease of the heart
Dysparunia arises from vaginal dryness and atrophic vaginitis. Local treatment with
estrogen creams relieves this problem.
Psychologic problems may arise from estrogen deficiency or from the effects of other
climacteric problems (hot flush and dysparunia). Symptoms include anxiety, insomnia,
irritability, depression, dementia and mood changes.
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Postmenopausal bleeding
It is defined as vaginal bleeding after 6 months of menopause. It is an abnormal condition
that always needs proper investigation. It could arise from benign conditions or more
seriously it may be a sign of serious malignant conditions of the genital tract. The causes are
Atrophic vaginitis
Atrophic endometritis
Cervical cancer
Endometrial hyperplasia and polyps
Endometrial cancer
Sarcoma of the uterus
Vulvar and vaginal cancer
Estrogen producing tumors
Exogenous estrogen therapy
Note: All women with postmenopausal bleeding should be referred for identification of the
cause.
Review questions
1. Define climacteric and describe the hormonal changes.
2. Describe the problems of climacteric.
3. List the causes of postmenopausal bleeding.
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CHAPTER 26
ABNORMAL VAGINAL DISCHARGE AND VULVAR PRURITIS
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Learning Objectives
To understand physiology of normal vaginal discharge
To list the causes of leucorrhea
To enumerate the causes of abnormal vaginal discharge
To discuss the clinical features, diagnosis and management of candidiasis
To discuss the clinical features and management of trichomoniasis
To discuss the clinical features and the management of bacterial vaginosis
To describe the causes of vulvar pruritis
VAGINAL DISCHARGE
1. .Definition
Normal vaginal discharge is defined as vaginal secretion which is scanty to moderate in
amount, non offensive, non purulent and non irritant. But to declare it to be normal and not
an infective one, requires clinical and laboratory investigations.
Abnormal vaginal discharge is abnormal condition where by the patient complains of unusual
vaginal secretion either in amount, odor, color or associated itching.
2. Physiology of vaginal discharge
The physiologic basis involved in normal vaginal secretion is dependent mainly on
endogenous estrogen level and to a lesser extent on endogenous progesterone level.
During follicular phase of menustral period, there is abundant secretary activity of the
endocervical glands, which secrete thin and clear mucoid secretion. In the presence of
progesterone it becomes thick and white. In the presence of estrogen, the superficial vaginal
epithelium becomes rich in glycogen. Following desquamation of theses cells, the glycogen
is changed to lactic acid by Lactobacillus deoderli, commonly called, the doderlein bacilli.
The resulting acidic PH of the vagina inhibits the growth of many bacteria.
3. Causes
I. Physiologic vaginal discharge - Leucorrhea
Excess discharge from the vagina not related to any pathology could occur in a variety of
conditions like
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Sexual stimulation with or without coitus
In the periovulatory period
Following menustration
Pregnancy
Cervical ectropion
II. Pathological vaginal discharge
Vaginal and cervical infections include candidiasis, trichomoniasis, bacterial vaginosis and
cervicitis (acute or chronic). This is the commonest cause of vaginal discharge.
Benign and malignant tumors of the vulva, vagina, cervix and the uterus
Atrophic vaginitis in climacteric
Foreign body with secondary infection
Rarely intestinal parasites migrating into the vagina (enterobiasis, amebiasis)
4. Vaginal Infections
4.1. Trichomonas Vaginalis Vaginitis (Trichomoniasis)
Etiology
This condition is caused by Trichomonas vaginalis, a motile protozoan. It is predominantly a
sexually transmitted organism. The male harbors the infection in the urethra and the
prostate. Rarely, it may be transmitted by fomites. The incubation period is 3- 28 days.
Incidence
It accounts for approximately 25% of vulvovaginal infections. About 20 -50% are
asymptomatic.
Clinical Presentation
The primary symptom is profuse and offensive vaginal discharge dating from the last
menstruation. It is often yellow – grey or greenish in color and frothy in character. Variable
degree of vulvar irritation and itching is present. Significant dysparunia is present.
Vaginal examination is painful. Examination will show thin greenish yellow and frothy
offensive discharge in the vagina. Vaginal walls are inflamed (red). Punctuate or strawberry
spots may be seen on the cervix and the vagina. Variable degree of vulvar soreness may be
seen. Abnormal Pap smear is seen in 70 % of the cases.
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Diagnosis
This made by identifying the flagellated trichomonads on wet mount of vaginal fluid. Culture
is only needed in resistant cases.
Treatment
Metronidazole is the drug of choice. It can be given as a single 2 gram dose or can be given
as 500 mg three times /day for 7 days. The partner should be identified and treated. During
pregnancy this drug should not be given in the first trimester. For persistent cases higher
doses or parenteral metronidazole can be used.
Complications
If untreated it may serve as a vehicle for STI agents to cause PID.
4.2. Candidal vulvovaginitis (moniliasis or candidiasis)
Etiology
In more than 80 % of the cases, it is caused by the fungi Candida albicans. This is a
dimorphic fungus with yeast and filamentous forms. In 20% Candida glabrata is responsible.
These organisms are normal flora of the lower gastrointestinal tract and the vagina in some
women.
Incidence and predisposing factors
75 % of women develop this infection sometime during their life time. In 40% it recurs.
Moniliasis is considered to be an opportunistic infection that arises when there is change in
the local or systemic defense mechanisms. The predisposing factors for such changes are
Pregnancy
Oral contraceptives
Diabetes mellitus
Broad spectrum antibiotics
Suppressed immune system like HIV/AIDS or use of steroids
Presence of local warmth and moisture
Clinical Features and diagnosis
The infection is asymptomatic in 20% of women. Intense vulvo-vaginal pruritis is the primary
symptom. Often it is associated with vaginal discharge. Typically the discharge is variable in
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amount, thick and curd like consistency, whitish in color and non offensive. The pruritis is
often out of proportion to the discharge. There may be superficial dysparunia and dysuria
due to local soreness.
Examination may show excoriated vulva. In severe cases it is swollen and red. Speculum
examination shows curd like discharge in flakes often adherent to reddened vaginal wall.
Scraping of these from the vaginal wall reveals bleeding points on the vagina. Vaginal PH is
acidic, often less than 5.2.
Balanopostaitis may be present in the coital partner. The most common complaints are
irritation of the glans penis and prepuce and itching of the scrotum.
Diagnosis is made by doing 5-10 % potassium hydroxide staining or wet mount of a sample
of vaginal discharge. This will show the yeast or the hyphae. In recurrent cases culture may
be needed.
Treatment
Systemic and local (suppositories or creams) antifungals are used to treat this condition.
Systemic antifungals are contraindicated during pregnancy.
Local antifungals: Nystatin, clotrimazole, miconazole, econazole
Systemic antifungals: Ketokonazole (200 mg / day for 10 days), fluconazole (150 mg once)
For recurrent cases treatment of male partner, identifying and treating the predisposing factor
and vaginal acidification are management options.
4.3. Bacterial vaginosis
This is a condition of the vagina in which there is an overgrowth of anaerobes with paucity of
lactobacilli and frequent absence of inflammatory cells. It has undergone nomenclature
changes over the years (nonspecific vaginitis, anaerobic vaginitis).
Etiology
Bacterial vaginosis is caused by a variety of facultative anaerobic organisms. Gardnerella
vaginalis is the most frequently associated organism. Others are mycoplasma hominis,
Bacteroides, peptostreptoccus and peptococcus.
Incidence
It accounts for 25- 30 % of vaginal discharges. In 50% it is asymptomatic.
Clinical features
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The most frequent complaint is a foul smelling, thin homogenous vaginal discharge with a
fishy smell. Often it is profuse, frothy and grayish. Pruritis is often minimal.
Examination will show normal vaginal mucosa with no sign of inflammation and thin offensive
discharge which is easily wiped from the vaginal wall.
Diagnosis
A positive amine test (the detection of a fishy smell when a drop of 10% KOH is added to a
drop of the vaginal discharge on a micro slide) and finding of clue cells on wet – mount
preparation made with 0.9% physiologic saline are diagnostic of bacterial vaginosis. Vaginal
PH is above 4.5. Gram stain of the vaginal discharge shows absent lactobacilli, numerous
gram variable bacteria and minimal leukocytes.
The diagnosis is confirmed if 3 of the following 4 criteria are present:
A grey – white vaginal discharge, which is sometimes foamy
Positive amine fish test
Positive clue cells
Vaginal PH of .4.5
Treatment
Metronidazole is the most effective treatment. The dose is similar to the dose used in
treatment of trichomoniasis. Other options are clindamycin and ampicillin. Acidification of the
vagina using acid gel or commercial yogurt (lyophilized lactobacillus acidophilus) is an option
in recurrent cases.
Complications
If untreated it is associated with PID, preterm labour, PROM and postpartum endometritis.
4.4. Gonococcal cervicitis
It is caused by Neisseria gonorrhea, a sexually transmitted organism.
It may not cause any symptoms. When symptomatic it manifests with mucopurulent, usually
non offensive and nonpruritic in nature. Speculum examination reveals inflamed cervical os
with mucopurulent discharge from the inside of the cervix.
Diagnosis is made by finding gram negative intracellular diplococci on gram stain of vaginal
discharge.
Management is treatment of both the woman and her partner with cephtriaxone 250 mg
intramuscular single dose or spectinomycin 2 gram intramuscular single dose.
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If untreated it may cause acute PID.
VULVAR PRURITIS
Vulvar pruritis is significant itching that is confined to the vulva. It is one of the commonest
presenting complaints in gynecology. It affects around 10 % of women.
In some cases the cause is easy to diagnose but in most arriving at the diagnosis poses
considerable difficult. The causes could be systemic illnesses or they could be local
conditions.
1. Etiology
I. Systemic causes
Unstable diabetes
Hepatobiliary diseases like biliary cirrhosis and cholestatic jaundice
Renal failure
Hematological conditions like polycythemia, anemia
Fat malabsorption
Systemic dermatosis like psoriasis, seborrheic dermatitis
Skin infections like scabies, pediculosis and tinia cruris
II. Local conditions
Vaginal discharge of any cause but mainly candidiasis
Atrophic conditions during climacteric
Allergic conditions from soap, contraceptive creams
Vulvar dystrophies and vulvar cancer
III. Psychosomatic
Note: Candidal vulvovaginitis is the commonest cause of vulvar pruritis.
2. Diagnostic work up
History should identify
The exact site of itching (vulvar, perianal or other sites in the body)
The duration
The nature - intermittent or continuous and progress over time
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Severity as related to lack of sleep or presence of excoriations
Presence of vaginal discharge
Drugs used
Medical illnesses and conditions causing allergy
Physical examination
General dermatologic examination
Inspection of the vulva and adjacent area (vagina, cervix, perianal areas) for discharge,
excoriation marks, ulcers and masses.
Investigations
This depends on the suspected cause and include;
Potassium hydroxide, gram stain and wet mount examination of vaginal discharge
Screening for diabetes, renal, biliary and hematological diseases
Work up of dermatologic illnesses
For persistent cases referral for biopsy to rule out dystrophies
Treatment
Treatment of identified systemic, dermatologic and local conditions
Appropriate local hygiene is to be taken care of. Avoid washing with soap or application of
perfumes. Vulvo – vaginal douching should be avoided. Use loose fitting undergarments
preferably made of cotton to keep the area aerated.
To prevent the vicious cycle of scratch itch scratch use local cortisol creams and sedation at
night. For atrophic conditions use estrogen creams.
Persistent cases should be referred.
6. Vulvovaginitis in childhood
Inflammatory conditions of the vulva and vagina are the commonest disorders during
childhood. Due to lack of estrogen, the vaginal defense is lost and the infection occurs
easily.
Etiology
Non specific vulvo vaginitis
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Presence of foreign body in the vagina
Associated intestinal infestations, thread worm being the commonest
Rarely more specific infection caused by Candida albicans or Gonococcus may be
implicated
Clinical features and diagnosis
The chief complaints are pruritis of varying degree and vaginal discharge. There may be
painful micturition.
Inspection reveals soreness of the vulva. The labia minora may be swollen and red. Vaginal
discharge varies from scanty to copious, at times offensive. If a foreign body is suspected a
rectal examination may help in diagnosis. If it fails to detect, examination under anesthesia
using an aural or nasal speculum is to be done.
In every case, the investigation regarding the cause is to be sought for. The vaginal
discharge is collected with a platinum loop and two smears are taken, one for direct
examination and the other for gram stain. A small amount may be taken with a pipette for
culture. To exclude intestinal infestation, stool examination is of help.
Treatment
In most cases, the cause remains unknown. Simple perineal hygiene will relieve the
symptoms. In cases of soreness or after removal of foreign body, estrogen ointment is to be
applied locally every night for 2 weeks. Alternatively, half tablet of ethinyl estradiol 0.01 mg
is to be given daily for three weeks to improve the local vaginal defense. When the specific
organisms are detected, therapy should be directed to cure the condition.
Review questions
1. Describe the causes of vaginal discharge.
2. Discuss the causes, clinical features and management of infectious vaginal discharge.
3. Discuss the causes of vulvar pruritis
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CHAPTER 27
PELVIC INFLAMMATORY DISEASE (PID)
Learning objectives
To define and classify pelvic inflammatory disease (PID)
To discuss the pathophysiology of PID
To discuss the diagnosis of acute PID
To list the complications of acute PID
To describe the management of acute PID
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Pelvic inflammatory disease (PID) is a clinical syndrome used to describe infection or
inflammation of the upper female genital tract above the level of the internal os of the
cervix often with involvement of the adjacent tissues.
This general term does not specify the site [endometrium (endometritis), fallopian tubes
(salphingitis), ovaries (oophoritis) and parametrium (parametritis)] or the stage (acute,
subacute, recurrent and chronic) or the etiologic agent.
Besides the site and stage, PID can be classified using the antecedent event
Postpartum PID (follows delivery)
Postabortal PID (follows abortion)
Port IUCD or instrumentation (follows IUCD insertion or diagnostic curettage or
hysterosalpingography)
Post operative (follows pelvic operations mainly after hysterectomy)
Post STD (follows sexually transmitted infections)
Secondary to other infections like appendicitis and tuberculosis
ACUTE PELVIC INFLAMMTORY DISEASE
1. Epidemiology
Acute PID is common problem affecting 1-2 % of women between ages 15 -35 years.
Incidence is increasing because of increasing antecedent events. Risk groups include
menstruating teenagers, those with multiple sexual partners, those using IUCD and those
with previous history of PID.
2. Physiological barriers
The upper female genital tract above the level of the internal os is sterile, despite the fact the
cervical canal and the vagina are colonized by millions of bacteria. The barriers that prevent
colonization of the upper female genital tract are
Cervical canal that is normally closed and is plugged by mucus
Presence of lysozyme and secretory IgA in cervical secretions
Cyclic shedding of the endometrium
Apposition of the chorion leave to the decidua during pregnancy
Downward beating of the tubal celia
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Systemic host defense
3. Pathogenesis
Microorganisms causing PID are not sufficiently mobile to reach the upper female genital
tract. Conditions that cause a breach in the physiologic barriers like childbirth or abortion or
IUCD insertion or surgery create conducive situation for PID to occur. But PID occurs
spontaneously in a woman having none of these conditions. Two theories are forwarded to
explain this
Vector transport theory – bacteria use vectors like spermatozoa and Trichomonas vaginalis
(a sexually transmitted agent), to transport them to the upper female genital tract
Pressure gradient theory – negative pressure in the uterus during orgasm sucks the
bacteria into the endometrium
Note: Coitus is a prerequisite for PID. It is rare to find PID in virgins, if found it is almost
always PID descending infection from appendicitis or pelvic tuberculosis from
haematogenous spread. PID in an intact pregnancy is also rare.
Once bacteria are inoculated into the endometrial cavity, bacteria proliferate and disseminate
to the other parts of the genital tract. Two routes of spread exist.
Direct upward canalicular spread (endometrial –endosalphingeal –peritoneal spread) most
common way of post STI (non puerperal) PID spread
Indirect parametrial - paracervical lymphatic spread is most common way of puerperal/
postabortal PID spread.
4. Etiology
It depends on the antecedent event.
Acute PID following abortion and delivery is a polymicrobial infection caused by organisms
ascending from the vagina. These are normal flora of the vagina which under normal
circumstances do not cause infection. Variety gram negative and positive, aerobic and
anaerobic organisms are involved. Common aerobic organisms include non hemolytic
streptococcus, E.coli, group B streptococcus and staphylococcus. Common anaerobic
organisms are Bacteroides fragilis and bivius, peptostreptoccus and peptococcus.
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Acute post STI PID is primarily caused by Neisseria gonorrhea or Chlamidia trachomatis.
Secondary infection may involve polymicrobial organisms.
Rarely exogenous organisms like clostridia may cause PID.
5. Clinical features and diagnosis
Clinical diagnosis of acute PID is often difficult because presentation varies widely and
symptoms are vague and non specific. Therefore, current criteria for diagnosis use
combination of physical signs rather than symptoms.
Typical cases of acute salphingitis present with bilateral lower abdominal pain (severe and
acute in gonococcal PID and dull and subacute in chlamydial PID) and fever with
constitutional symptoms like malaise, headache nausea and vomiting which usually start in
few days after menustration.
The typical physical findings are pyrexia, tachycardia, lower abdominal direct and rebound
tenderness, cervical excitation tenderness and bilateral adenexal tenderness. These findings
are less pronounced in chlamydial PID.
Laboratory investigations reveal leukocytosis of more than 10,000/cc, an elevated ESR
value of more than 15 mm per hour and high white cell count and positive gram stain/ culture
in culdocentesis aspirate. In early uncomplicated cases ultrasound and gram stain of vaginal
discharge are of little help.
According to the Hegar criteria clinical diagnosis of acute PID is made when all major
criteria plus at least one minor criterion are found.
I. Major criteria:
Lower abdominal pain with direct and/ or rebound tenderness,
Cervical excitation tenderness,
Adenexal tenderness
II. Minor criteria:
Fever of >380c,
WBC count of >10,000/mm3 or ESR of >20 mm/hour,
Positive gram stain for gonorrhea or >5 WBC/ oil immersion field from cervical discharge,
Culdocentesis shows purulent fluid or WBC with bacteria on gram stain
Inflammatory mass or abscess on pelvic examination or ultrasound
Clinically acute PID can be graded into three.
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Grade I: PID limited to the adnexa
Grade II: PID with inflammatory mass or abscess
Grade III: Ruptured tuboovarian abscess with generalized peritonitis
6. Differential Diagnosis
Clinical conditions that mimic acute PID include appendicitis, ectopic pregnancy, torsion of
ovarian cyst, hemorrhage or rupture of ovarian cyst, urinary tract infections and less common
conditions like endometriosis.
7. Complications
If early diagnosis is not made and aggressive therapy is not given, acute PID progresses to
cause serious and debilitating complications including death. The immediate
complications are
Pelvic peritonitis or even generalized peritonitis with ileus
Septicaemia producing metastatic infections, like arthritis and endocarditis
Septic shock ending up in multiple organ failure
Pelvic abscess and tuboovarian abscess
Infectious perihepatitis (Fitz – Hugh – Curtis syndrome)
Complications of surgical management
The late complications are
Infertility – overall rate is 25% but risk increases with the number of attacks.
Ectopic pregnancy – increased by 6-10 folds
Chronic pelvic pain with dysparunia and dysmenorrhea
Intestinal obstruction
8. Management
The goals of therapy are controlling acute infection, preventing long term complications and
re-infection. Treatment of acute PID can be given as outpatient or inpatient. The indications
for inpatient management are:
Severe toxic: temperature of >390c with lower abdominal tenderness/guarding
Current pregnancy
Patient known to have HIV/ AIDS
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Suspected or proven tuboovarian abscess
Failure of response to outpatient treatment in 48-72 hours
Noncompliance or non tolerance to outpatient treatment
Uncertain diagnosis in which surgical conditions can not be ruled out
I. Outpatient management
Apart from adequate rest and analgesic, antibiotics should be prescribed even before the
microbiological report is available. Because the infection is poly microbial in nature,
combination of antibiotics should be prescribed.
There are many different antibiotics regimens, but the spectrum of activity of the antimicrobial
agents should cover the following organisms: Neisseria gonorrhea, chlamydia trachomatis,
aerobic and anaerobic organisms. Follow up visit should be arranged after 72 hours, 7days
and 3 weeks.
II. Inpatient management
General or supportive care includes intravenous or oral hydration, bed rest in semi fowler’s
position and administration of analgesic/ antipyretic.
The specific treatment is administration of intravenous combination antibiotics that cover
Neisseria gonorrhea, Chlamydia trachomatis, aerobic and anaerobic bacteria. Clinical
response is evidenced by remission of temperature, improvement of pelvic tenderness,
normal white blood cell count and negative report on bacteriological study.
Indications for laparatomy are worsening condition of the patient, generalized peritonitis,
pelvic abscess and if other surgical conditions (appendicitis, ectopic pregnancy) can not be
ruled out.
9. Prevention
Early detection and treatment of STI including asymptomatic cases like gonococcal cervicitis
Partner identification and treatment (contact tracing)
Safe sexual practices including condoms and avoiding multiple partners
Review questions
1. Define and classify PID.
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2. List the major and minor Hegar criteria.
3. Describe the management of acute PID.
4. List the complications of acute PID.
CHAPTER 28
FAMILY PLANNING
Learning Objectives:
To list the different types of contraceptive methods
To describe the natural family planning methods
To list the different types of barrier methods
To describe the side effects of IUCDs
To describe the different types of hormonal methods
To describe the surgical contraceptive methods
Introduction
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The term contraception includes all measures, temporary and permanent, designed to
prevent pregnancy. On the other hand, the term family planning (fertility control) includes
both fertility inhibition (contraception) and fertility stimulation.
Rapid population growth is a critical issue in most developing countries. Family planning
methods save women’s lives by preventing unintended pregnancies. Slower population
growth conserves resources, improves health and living standard.
Ideal contraceptive methods should be widely acceptable, inexpensive, simple to use, safe,
highly effective and requiring minimal motivation, maintenance and supervision. So far there
is no universally acceptable method.
Methods of Contraception are divided into
Natural family planning method
Barrier methods
Intrauterine contraceptive device
Hormonal contraception
Surgical contraception
The effectiveness of contraceptive method can be measured by the pearl index. The Pearl
Index is a figure which is obtained by using the pearl formula and it indicates the number of
pregnancies which would occur if 100 women use a specific method for one year.
The pearl index of the pregnancy figure per 100 women years of use =
100 (women) * 12 (ovulations per year) * number of pregnancies / total months of use.
Failure rate is further less when methods are used correctly and consistently.
Clients have to be counseled about all the available family planning methods and should
make their own choice. This is called informed choice and is usually reached by the
GATHER approach.
G stands for greeting
A stands for asking the client needs
T stands for telling the client about all the methods
H stands for helping the client to make the choice
E stands for explaining about the chosen method
R stands for return visit or referral to the facility that gives the services
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A. NATURAL FAMILY PLANNING
1. Rhythm method (Periodic abstinence)
The technique used in this method is confining sexual intercourse to the phases of menustral
cycle where conception is unlikely to occur. It needs identification of the fertile (unsafe) and
infertile (safe) phases of the menustral cycle. The fertile (safe) period extends from 4 days
before to 4 days after ovulation. The rest of the menustral cycle is infertile (safe) period. This
is based on the fact that a human ovum can not be fertilized no later than 48 hours after
ovulation and the human spermatozoa can not fertilize an ovum 48 hours after ejaculation.
Since there is no sign or test to tell the exact time ovulation, various methods are used to
determine the approximate time of ovulation and fertile period. These methods include.
I. The calendar method
This method requires recording the length of 12 consecutive menustral cycles. The beginning
of the fertile phase (first unsafe day) is calculated by subtracting 18 from the shortest cycle.
The end of the fertile phase (the last fertile day) is calculated by subtracting 11 from the
longest cycle. Sexual intercourse is abstained between these dates. User effectiveness is 20-
30 per 100 women.
II. The temperature method
This method requires measuring the basal body temperature before rising from the bed daily
staring from the first day of the menustral cycle. Sexual intercourse is abstained from the start
of the menustral cycle to 3 days after the record of temperature rise. User effectiveness is 20-
30 per 100 women.
III. The cervical mucus or Billings method
This method requires observing the cervical secretions daily by wiping the introitus with white
toilet tissue paper. Sexual intercourse is abstained from the onset of menses to 4 days after
maximum secretion of the cervical mucus. User effectiveness is 15- 20 per 100 women.
IV. Symptothermal method
This method is a combination calendar and temperature methods. In this method the first day
of abstinence is predicted by using calendar method and the last day by temperature method.
2. Coitus Interruptus (Withdrawal method)
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This method requires withdrawal of the penis from the vagina prior to ejaculation which must
occur outside the vagina and away from the immediate perivaginal area. This needs high level
of motivation and is associated with high failure rates.
3. Lactational amenorrhea method
Prolonged and sustained breast feeding offers a natural protection against pregnancy. This is
more effective in women who are amenorrhic that those who are menstruating. The risk of
pregnancy in the first 6 months in a woman who is fully breast feeding and amenorrhic is less
than 2 percent. Higher failure rates are observed in women who are breast feeding and are
menstruating. Protection gradually decreases after 6months.
B. BARRIER AND CHEMICALS METHODS
1. Condoms
These are thin sheaths made of latex. The male condom is put on a fully erect penis and
removed after ejaculation before the penis is deflated. The female condom is unrolled into
the vagina before sexual intercourse. Concomitant use of spermicidals improves
effectiveness.
Besides its contraceptive effectiveness, it also protects against STI and HIV/AIDS. It is useful
for couple with infrequent sexual intercourse.
Disadvantages are condom breakage, condom slippage, occasional allergy to latex and
claim of dulling of sexual sensation.
User effectiveness ranges from 6- 30/ 100 women and is mainly from improper and
inconsistent use.
2. Diaphragm
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This is a shallow dome shaped rubber cup with flexible rim. It has different sizes. It is
designed to fit behind the pubic bones, the lateral vaginal walls and the posterior fornix, thus
covering the external os of the cervix.
It is correctly placed in the vagina before sexual intercourse and is removed 6-8 hours after
sexual intercourse. Spermicidal jelly is applied to the inside and outside surface before
placement in the vagina.
It is advantageous to those who practice sex infrequently. The disadvantages are the
inappropriateness of the method and the increased incidence of urinary tract infections and
vaginal laceration.
The user effectiveness is 10- 20/ 100 women.
3. Cervical cup
This is a rubber cup with metallic rim designed to fit the cervix. It is applied to the cervix
before intercourse and provides continuous protection for 48 hours. It is not frequently used.
4. Spermicidals
This method involves deposition of spermicidal chemical (nanoxynol 9) into the vagina 10- 15
minutes before each sexual act. The various preparations include aerosol foams, creams,
foaming tablets and contraceptive sponges.
They also offer protection against STI and HIV/AIDS. The disadvantages are
inappropriateness, allergy, and presumed risk of congenital malformation.
The user effectiveness ranges between 2- 40/ 100 women.
C. INTRAUTERINE CONTRACEPTIVE DEVICES (IUCD)
This is a long term reversible contraceptive method involving insertion of a specially made
devise into the uterine cavity to offer constant protection against pregnancy.
A variety of devises have been used over years. The nonmedicated IUCDs, also called the
loop, are no more used nowadays. They have larger size and do not need regular
replacement. The medicated IUCDs contain either copper or progesterone that increases
their contraceptive effectiveness. They are smaller in size and need regular replacement.
Currently used medicated IUCDs are copperT380A (replaced every 8-10 years) and the
progestasert (replaced every year).
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The mechanism of action is not clear but is believed to be related to the sterile inflammatory
reaction in the endometrium, asynchronous development of the endometrium and interference
of the enzymes involved in implantation. Altered tubal motility, formation of thick cervical
mucus and maintenance of decidualized endometrium are additional mechanisms in
progestasert. IUCDs do not inhibit ovulation and fertilization.
The absolute contraindications are suspected or proven pregnancy, acute PID or purulent
cervicitis, unresolved abnormal uterine bleeding, uterine anomaly or myoma and cervical or
uterine malignancy. Relative contraindications are history of dysmenorrhea or
hypermenorrhea, valvular heart disease, bleeding disorders, impaired immunity (HIV/AIDS or
diabetes), nulliparous woman, previous ectopic pregnancy and women with multiple sexual
partners.
The side effects / complications are perforation, cramps and syncopal attack during insertion,
hypermenorrhea, dysmenorrhea, ectopic pregnancy and PID. Spontaneous expulsion may
occur.
Depending on the timing, there are three type of IUCD insertion: Interval (insertion made in a
non pregnant woman or after 6 weeks postpartum or abortion), postabortal (immediately after
abortion) and postpartum (immediately after delivery). Interval insertion can be done at any
time of the menustral cycle as long as pregnancy is ruled out, but the best time is during
menustration or within 7 days of the menustral cycle. IUCD insertion is an out door procedure
and can be done even by a trained paramedical personnel without anesthesia.
Indications for removal are suspected perforation, persistent cramp after insertion,
hypermenorrhea causing anemia, severe dysmenorrhea, PID, pregnancy, displacement of
the IUCD, missing thread and client request.
User effectiveness is 1-3 %.
D. HORMONAL CONTRACEPTION
1. Combined Oral Contraceptives (The Pill or OCPs)
The combined oral steroidal contraceptive is a very effective short term reversible method of
family planning. It contains both estrogen and progesterone derivatives in a single tablet.
There are two types of formulations. The multiphasic pills have tablets with varying amount
of estrogen and progesterone in different rows. The monophasic pills have the amount of
estrogen and progesterone in all the tablets. Depending on the amount of estrogen, the
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258. Obstetrics and Gynecology
monophasic pills are further subdivided into low dose (if the amount of ethinyl estradiol is <
0.05 mg) and standard dose (the amount of ethinyl estradiol is 0.05 mg). The commonly
used progestins are levonorgestrel, norethisterone and lynosterol. The estrogens are either
ethinyl estradiol or menstranol.
The mechanism of action of OCPs is mainly by inhibition of ovulation but thickening of
cervical mucus, decidualization of the endometrium and alteration of motility of the fallopian
tubes also contribute.
The absolute contraindications are proven or suspected pregnancy, undiagnosed abnormal
uterine bleeding, coronary artery disease, history of stroke or thromboembolism, active liver
disease, liver adenoma, estrogen dependent neoplasm, breast cancer, and smoking over the
age of 35 years. The relative contraindications are breast feeding, migraine headache,
history of cholestasis, severe hypertension, diabetes mellitus, varicose veins and elective
operation in 4 weeks. Epilepsy, and anti Tb treatment are relative contraindications because
of accelerated clearance of the hormones.
The side effects are nausea, vomiting, weight gain, headache, breast soreness, acne,
chloasma, and mild hirsutism, mood changes like depression, break through bleeding, post
pill amenorrhea, leucorrhea, vaginal candidiasis, headache and decreased amount of breast
milk.
The complications which occur in those with risk factors are vascular thrombosis and
embolism, myocardial infarction, stroke, hypertension, liver tumors especially hepatic
adenoma and cholelithiasis.
The danger symptoms that indicate discontinuation are severe migraine, visual disturbance,
sudden chest pain, severe cramps and swelling of the legs, severe right upper quadrant pain
or jaundice and breast lump.
Additional indications for discontinuation are excessive weight gain, client wish to conceive,
client request and planned elective surgery.
Non contraceptive benefits of OCPs are relief of menorrhagia, relief of dysmenorrhea, relief
of dysfunctional uterine bleeding and premenstrual syndrome, improvement of iron deficiency
anemia and endometriosis. It is also associated with marked reduction in the risk of pelvic
inflammatory disease (protective thick cervical mucus), benign breast disease, fibroid uterus,
carcinoma of the endometrium, carcinoma of the ovary and osteoporosis.
2. Progestin only pill (Minipill or POP)
These pills contain only progesterone derivatives in very low dose. The progestins commonly
used are levonorgestrel 75 mg, norethisterone 350 mg, ethinodiol diacetate 500 mg,
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259. Obstetrics and Gynecology
desogestrel 75 mg, lynosterol 500 mg, or norgestrel 30 mg. They have to be taken
continuously with no hormone free interval.
They are useful for women in whom estrogen containing contraceptives are contraindicated.
The mechanism of action is mainly by cervical mucus thickening, decidualization of the
endometrium and changing tubal motility. Ovulation suppression is partial and occurs in only
50 %.
The advantages include elimination of side effects attributable to estrogen like thrombosis
and change in lipid profile and absence of adverse effect on lactation and milk volume.
Because of these advantages POPs can be prescribed to lactating women and women with
hypertension, thrombosis, diabetes and smokers.
The disadvantages are increased incidence of menustral changes like breakthrough bleeding
and in some amenorrhea, very low dose contraceptive with increased failure rate especially if
pill is missed or taken late, increased risk of ectopic pregnancy and ovarian cyst formation.
Because of the very low dose nature of these contraceptives and the partial suppression of
ovulation, patients should be counseled about the importance of taking the pills at the same
time of the day and the dangers of missing the pill. A back up method like barrier methods
have to used in the first month, if the menustral cycle is regular, if there is delay in taking the
pill on time or if missed and if a woman is taking drugs that accelerate clearance of the
progesterone from the body like anti epileptics and anti TB drugs.
Failure rate is about 0.5 – 2 per 100 women years.
3. Injectables contraceptives
These are long acting reversible contraceptives containing progesterone preparations.
Preparations commonly used are depomedroxy progesterone acetate (DMPA), also called
Depo-Provera and norethisterone enanthate (NET-EN). Both are administered
intramuscularly; DMPA in a dose of 150 mg every three months or 300 mg every six months
and NET – EN in a dose of 200 mg given at two months intervals. They are administered by
deep intramuscular injection. The site of injection should not be massaged. There is a grace
period of 2 weeks for Depo-Provera, in which the client may be late for injection without
increased risk of pregnancy. This does not work for NET-EN.
The mechanism of action is mainly by inhibition of ovulation by suppressing the mid cycle LH
peak. Additional effects include cervical mucous thickening and endometrial atrophy which
prevents blastocyst implantation.
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The advantages are similar to that of the mini pills. In addition injectable contraceptives avoid
the need of daily administration of the drugs. It causes amenorrhea thus relieves menustral
disorders like menorrhagia and dysmenorrhea. It is not affected by gastrointestinal functions.
Because it is not visible, it is culturally acceptable in most settings. It protects against
endometrial cancer. Unlike other hormonal contraceptives, it is devoid of drug interactions
like antiepileptics.
The disadvantages are related to the side effects that it causes. These include weight gain,
headache, and back pain, loss of hair and mood changes. There is delay in return of menses
and fertility of upto 8 months after discontinuation. The other disadvantage is once the drug
is injected it can not be retrieved, thus side effects can not be reversed promptly.
Failure rate for DMPA is < 1% per hundred women year.
4. Implants (Norplant)
Norplant is a long term, extremely low dose reversible progestin only contraceptive method
that is effective for a period of 5 years.. It has six silastic rubber capsules each containing 36
mg of levonorgestrel. This hormone is released by slow diffusion over a period of five years.
It is placed sudermally in a fan like manner into the inner aspect of the nondominant arm by
sterile minor surgical procedure.
The mechanism of action is similar to Depo-Provera. It inhibits ovulation in 90% of the cycles
for the first year. This effect gradually wanes as the years of use increase.
The advantages are similar with Depo-Provera. Unlike Depo-Provera, it is effects are
immediately reversed upon removal. There is no delay in return of fertility. It is suitable for
women who have completed their family but do not desire permanent sterilisation.
The disadvantages are procedure related like the need for professional for insertion and
removal, need for minor surgical procedure, inflamation and infection at the insertion site and
visibility of the implants. It has also higher initial cost. Failure rate is increased in women
taking anticonvulsants and anyiTB drugs. Breakthrough bleeding may be troublesome. Other
side effects like weigh gain, mood changes ,hair loss and back pain are common.
The indications for removal are prergnancy, client request, infection at the site of insertion,
spontanous expulsion of one or more of the implants, after 5 years of use, and development
of serios side effects like migraine headache, bluuring of vision, unilateral leg pain and
swelling and chest pain.
Failure rate is 0.1 per 100 women years which increases with years of use.
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E. VOLUNTARY STERILIZATION (SURGICAL CONTRACEPTION)
Surgical contraception is a permanent method of contraception. The operation done on male
is vasectomy and that on the female is bilateral tubal ligation (occlusion). It is important
to explain to the clients that all operative sterilizations are intended to be permanent.
Consent for the operation should be signed after counseling.
1. Male voluntary sterilization- Vasectomy
It is a permanent sterilization operation done in the male, where a segment of both vas
deferens is resected and the cut ends are ligated. It is a simple outdoor minor surgical
procedure requiring minimal training.
Immediate and late complications are few. Impotence mainly of psychological nature may
develop. It does not increase the risk of testicular cancer. Failure rate is 0.15% and there is a
fair chance of success of reversal anastomosis operation (50%).
The procedure is not immediately effective. It usually takes 2-3 months or about 20
ejaculations before the semen is free of spermatozoa. Therefore, additional contraceptive
protection is needed for about 2-3 months following operations. Confirmation by semen
analysis is needed after 3 months.
2. Female voluntary sterilization- tubal ligation
Occlusion of the fallopian tubes is the most popular method of surgical contraception,
especially in areas where high parity births prevail in a comparatively younger age group. It
is also widely accepted in the affluent countries. The procedure is immediately effective.
Timing of operation
Postpartum tubal ligation - If the patient is otherwise healthy, the operation can be done 24 –
48 hours following delivery. Its chief advantage is technical simplicity.
Postabortal tubal ligation - Sterilization performed along with elective abortion.
Interval tubal ligation – The operation is done after 3 months following delivery or after 3
weeks following abortion. The ideal time of operation is following the menstrual period in the
proliferative phase.
It can be done during caesarian section or by minilaparatomy or by laparoscope. Either
ligation methods or mechanical occlusion or electro coagulation are used to occlude the
tubes. There are various techniques of ligating the tubes, the commonest one being the
Pomeroy method.
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Failure Rate in tubal sterilization is about 0.7%.
F. EMERGENCY CONTRACEPTION
This is a kind of contraception that is used in the prevention of pregnancy following an
episode of unprotected intercourse during the fertile period. It used to be called morning
after pill or post coital pill.
There are two types of emergency contraception.
I. Hormonal emergency contraception
These act by temporarily disrupting ovarian hormone production causing absent or
dysfunctional luteal phase. This results in development of out of phase endometrium that is
not suitable for implantation.
They have to be taken within 72 hours of unprotected intercourse. There are a variety of
regimens. The commonest one is Yuzepe regimen. In this method two doses of
combination of ethinyl estradiol and norgestrel is taken 12 hours apart. The first dose should
be taken as early as possible as but no later than 72 hours after intercourse. The total dose
of ethinyl estradiol is 0.2 mg and that of norgestrel should be 2 mg (2 tablets of standard
dose pills like Ovral taken 12 hours apart).
The side effects are nausea, vomiting, breast tenderness, headache and menustral
disturbance. Incidence of ectopic pregnancy is increased. Therefore, women should be
counseled to report if they miss their menses and develop lower abdominal pain.
II. Mechanical emergency contraception
This involves inserting an intrauterine devise within 5 days of unprotected intercourse.
Review Questions
1. Describe the GATHER approach.
2. Describe the natural family planning methods.
3. Describe the different barrier methods.
4. List the contraindication for combined pills.
5. Describe the complications of IUCD.
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6. Describe the norplant.
7. Describe the emergency contraception.
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CHAPTER 29
INFERTILITY
Learning objectives
To define and classify infertility
To list the causes of infertility
To describe the diagnostic work up of infertile couple
To list the management modalities of infertility
1. Definition and classification
Infertility is failure of a woman to conceive after one year of unprotected intercourse (without
contraception) if the woman is >35 years and after two years if the woman is <35 years.
There are two types of infertility
Primary infertility - if conception has never occurred before.
Secondary infertility - if there was history of pregnancy before the current problem,
irrespective of its site and outcome.
2. Epidemiology
Incidence varies according to the socioeconomic and geographic factors. Globally 8 - 12%
couples face problem of infertility in their life time. In sub-Saharan Africa the incidence rises
to 20 - 30% where around 8-10 million women are estimated to be infertile. In addition to the
personal psychosocial trauma (shock, denial, depression), infertility has an impact in the
couple’s relations that can lead to marital disharmony and divorce.
3. Etiology
In 85- 90% of infertile couple a probable cause is found. In 10-15% the infertility is
unexplained. The causes of infertility could arise either from the female or the male or both.
According to WHO, male cause accounts for 8-22%, female cause accounts for25-37% and
both partners are responsible for 21 – 38%.
Globally the most common causes are:
Tubal factor, which accounts for 20- 30 % of infertility, arises from congenital or acquired
obstruction of the fallopian tubes. Acute PID is the commonest cause of tubal obstruction.
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Male factor, which accounts for 15-25% of infertility, arises either from failure of
spermatogenesis (testicular failure) or more commonly from obstruction of the vas deferens.
Gonococcal infection is the commonest cause of obstruction of the vas deferens.
Ovulatory factor, which accounts for 10-15% of infertility, arises from any condition that
cause anovulation. This may arise from disease conditions affecting the hypothalamus,
pitutary and the ovaries.
Pelvic factor, which account for 10% of infertility, is mainly the result of endometriosis.
Cervical factor, which account for 15% of infertility, arises from structural abnormality of the
cervix (like cervical atresia and stenosis) and functional abnormality of cervical mucus (like
cervicitis, hormone deficiency or colonization by mycoplasma).
Immunologic factor occurs as the result of development of antisperm antibodies by the
woman or her partner.
4. Diagnostic evaluation
The goals are detection of a possible cause, providing accurate information about prognosis,
providing guidance on treatment options and providing continuous counseling.
The approach should ideally include both partners at the initial assessment. Joint interview of
couple should be followed by separate private consultation. Based on the findings a variety
of investigations are ordered.
I. Evaluation of male partner
History: age, previous paternity, sexual history (technical difficulty, history of STI,
malformations of penis), medical history (trauma, mumps, chronic medical illness, prolonged
febrile illness), drug history (including alcohol and smoking), surgical history (mainly inguinal
and scrotal), occupation (toxins, prolonged heat) and review of systems (breast enlargement,
headache, exercise), previous tests and results.
Physical examination: general appearance, male habitus, hair distribution, breast
enlargement, voice, external genitalia (penis and scrotum), rectal examination (prostate).
II. Evaluation of female partner
History: age, menustral history (including ovulatory symptoms like mid cycle pain,
dysmenorrhea, breast pain), contraceptive history (duration, type, date of last use), obstetric
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history (especially on abortion, ectopic pregnancy, post partum hemorrhage), sexual history
(frequency, regularity, timing around mid cycle, STI, PID), surgical history (especially pelvic
operation), medical history (medical illness, breast discharge), drug history (type, duration),
review of systems (diet, weight, exercise)
Physical examination: general appearance, thyroid, secondary sexual characteristics, breast
discharge, uterine/ adenexal mass, uterine position and mobility, adenexal tenderness, visual
fields
III. Investigations
A. Baseline for both partners
Hemtocrite, white cell count, ESR, urinalysis, VDRL, fasting blood sugar
B. Investigations for the male
Seminal analysis
This is the most important fertility evaluation for the male. A normal test usually excludes
significant male factor. An abnormal result must be repeated after 3 months. The test is done
after 3-7 days of abstinence. Specimen should be examined within 60 minutes of collection.
Normal parameters are volume of 2- 6 ml, total sperm count 20 – 250 million /ml, sperm
motility of > 60% by subjective methods, sperm morphology of > 50% normal and celularity
of < 10 WBC / ml without significant agglutination. Of these the most important parameters
are the sperm count and motility.
Extended tests
These are done for those with abnormal seminal analysis. These include endocrine assay
(TSH, T3 /T4, FSH, LH, testosterone, prolactin), skull X-ray for sella turcica, sperm antibody
testing and others.
C. Investigations for female
Documentation of ovulation
History suggestive of ovulation is midcycle pain, premenstrual molmina and primary
dysmenorrhea. Indirect tests of ovulation determine the presence of sufficient amount of
progesterone in the body. These tests are recording the basal body temperature for three
cycles (biphasic shift), determining midluteal phase serum progesterone level (> 25ng//L),
endometrial biopsy at 21st day of the cycle( secretary endometrium), cervical mucus
examination after expected time of ovulation ( thick, yellowish with no ferning) and vaginal
cytology for maturation index.
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Hysterosalpingography (HSG)
This assesses tubal patency. It is done in the early part of the follicular phase.
Post coital test (Sims Hunner Test)
This assesses the cervical factor. It is done by aspirating cervical mucus from the cervical
canal at the level of the internal os 2–4 hours after sexual intercourse. A satisfactory result is
finding of >10 motile spermatozoa with good forward movement under high power field in the
presence of adequate cervical mucus.
Other tests
These include endocrine assay for anovulatory women (TSH, T3 / T4, FSH, LH, estradiol,
prolactin levels), laparoscopy/ laparatomy for assessing pelvic factors), determination of
sperm antibodies and others.
5. Management
Management depends on the specific cause.
Male factor infertility
It is directed against the cause.
There is no treatment for azospermia from primary testicular failure. Azospermia from
secondary testicular failure is treated by hormone replacement (GnRh agonists and human
menopausal gonadotrophins). Azospermia from obstruction of the vas deferens can be
treated by microsurgical vasovasotomy or by aspiration of the sperm followed by invitro
fertilization.
A number of interventions to improve the quality of the sperm have been used in those
abnormal or border line oligospermia or asthenospermia. These include drags like
clomiphene citrate or bromocryptine, surgery for varicocele, exercise modification, change in
occupation, abstinence from alcohol and smoking and avoiding hot baths. Treatment with
testosterone has limited value.
Other interventions include surgical correction of hypospadias and epispadias.
Female factor infertility
I. Anovulation: ovulation induction by clomiphene citrate. Other drugs like human
menopausal gonadotrophins are not available in Ethiopia. Underlying medical causes like
hyperprolactinemia and hypothyroidism have to be treated with appropriate drugs.
II. Tubal factor: surgical correction by tuboplasty
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III. Cervical factor: antibiotics like erythromycin and tetracycline for cervical infection and
colonization by mycoplasma, hormonal treatment for inadequate cervical mucus
IV. Immunologic factor: modalities of treatment that are tried include occlusive therapy by
condom for 6- 9 months, immune suppression by steroids, suppression of spermatogenesis
and intrauterine insemination.
Other treatment options
These should be offered to couple in whom treatment for infertility fails. They include
adoption, and where feasible assisted reproductive technology and serrogation.
Review Exercises
Define infertility and describe its types.
Discuss causes of infertility and their diagnostic methods.
3. Briefly describe the management modalities of infertility.
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CHAPTER 30
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TUMOURS CONDITIONS OF THE FEMALE GENITAL
TRACT
Learning Objectives
To know the epidemiologic features of genital tract tumors
To know the approach to patients with genital tumors
To understand the general principles and management options genital tract tumors
Like any organ system in the body, a variety of benign and malignant tumors develop in the
female genital tract. No part of the genital tract is immune for tumors, but the relative
frequency varies. In most the exact cause is unknown. The manifestations are varied and
range from absence of symptoms to symptoms affecting local or distant organs. Depending
on the site, the common presenting complaints are abnormal vaginal bleeding,
postmenopausal bleeding, abnormal vaginal discharge, vulvar/ abdominal mass, pruritis and
pelvic/ abdominal pain. The diagnostic modalities include cytologic studies, histopathological
studies and other advanced investigations like tumor markers and computerized tomography.
The management options are surgical excision, radiotherapy and chemotherapy.
BENIGN CONDITIONS OF THE FEMALE GENITAL TRACT
1. Vulva
White lesions include lichen sclerosis and hyperplasic dystrophy.
Hidradenoma: are lesions originating from the apocrine sweat glands. They are seen in
women in their twenties and thirties.
Pigmented nevus occurs on the vulva. It carries a risk of subsequent malignant
transformation due to junctional activity. Thus, excisional biopsy should be performed on all
pigmented lesions on the vulva.
Fibromas are uncommon and when present in the vulva are usually fibromyomas or
fibroangioma.
Hemangioma Vulva may be
Ulcerative lesions could arise following trauma or may be a manifestation of STI (syphilis,
chancroid, granuloma inguinale, lymphogranuloma venereum, and genital herpes) or may be
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a sign of systemic condition (Crohns disease and Bahcets disease). Persistent ulcerative
condition of the vulva should arouse suspicion of vulvar cancer and should be biopsied.
2. Vagina
Inclusion cyst
Gartner (mesonephric) duct cyst
Endometriosis
Adenosis
3. Cervical polyp
Cervical polyp is a localized overgrowth of the endocervical glands. It manifests with
abnormal vaginal discharge, intermenustral bleeding and contact bleeding. Speculum
examination shows a polypoid soft mass protruding through the cervical os. Management is
polypectomy.
4. Endometrial polyp
Endometrial polyp is a localized growth of the endometrium which could be sessile or
pedunculated. In some cases it may be long enough to protrude through the cervix where it
may be confused with cervical polyp. It may be asymptomatic. Symptoms include
intermenustral bleeding, menorrhagia and if it protrudes through vaginal discharge. Physical
findings are minimal. Diagnosis is made by hysterosalpingography or hysteroscopy. Removal
by dilatation and curettage is the treatment.
5. Uterine liomyoma (Fibroids, Myoma)
5.1. Definition and classification
Liomyoma is a benign tumor of the smooth muscle cells of any mullerian duct organs
especially the myometrium often with some admixture of fibrous tissue. It could be single or
multiple. Size ranges from 1mm to 20 cm in diameter. Depending on the location liomyomas
are classified as
Interstitial or intramural myoma is located in the myometrium and accounts for 70 % of
myomas.
Submucus myoma is a myoma that grows into the endometrial cavity. When a submucus
myoma protrudes into the cervical canal and the vagina it is called delivered myoma.
Subserous myoma is a myoma that grows to the serosal surface, thus distorts the surface
of the uterus. Sometimes a subserous myoma gets detached from the uterus and gets its
blood supply from another intraabdominal organ especially the omentum. This kind of
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myoma is called parasitic myoma. A subserous myoma that grows between the leaves of
the broad ligament is called intraligamentary (broad ligament) myoma.
Cervical myoma is a myoma that grows on the cervix.
5.2. Epidemiology and etiology
It is the commonest tumor of the uterus. It is found in 20-25 % of women in reproductive age
group. It is more common in blacks.
The etiology of myoma is unknown. But translocations and additions of several
chromosomes, mostly affecting chromosome 12 is observed in myomatous cells. Growth of
myoma is related to the presence of estrogen. This explains why myomas are rare before
puberty and why they atrophy after menopause.
5.3. Secondary changes
Myomas usually have a firm consistency and are non tender. But with subsequent growth,
they undergo secondary changes, which give them a varied consistency.
Hyaline degeneration gives it a soft consistency.
Cystic degeneration gives it a cystic consistency.
Fatty degeneration usually occurs after menopause and is a precursor for calcareous
degeneration.
Calcareous degeneration (womb stone) occurs when calcium is deposited in the myoma.
This gives it a hard consistency.
Red (carneous) degeneration occurs as the result of ischemic necrosis from obstruction of
the venous return during pregnancy. This results in tender swelling of the myoma. It resolves
in 1-2 weeks.
Sarcomatous degeneration is a malignant transformation of a myoma. It should be
suspected when there is significant growth of a myoma in a short period associated with
pain. It usually occurs in postmenopausal women. The incidence is 1:1000.
Suppurative (infective) degeneration usually occurs in submucosal types.
5.4. Clinical features
Symptoms depend on the site of the myoma. Approximately 35- 50% of myomas are
asymptomatic. Symptoms are varied and include:
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Abnormal uterine bleeding is the commonest presenting symptom. It usually takes the form
of menorrhagia and may cause significant anemia. Intermenustral and contact bleeding may
occur in delivered myoma.
Pressure symptoms like frequency of urination, intermittent overflow incontinence (urinary
bladder), constipation (rectum), pelvic pain (pelvic nerves, torsion, red degeneration), edema
of the extremity (vena cava or iliac vein) or flank pain (hydronephrosis from ureteric
obstruction).
Painless gradually enlarging suprapubic mass
Abnormal vaginal discharge in submucus type
Pelvic pain from torsion, infection, red degeneration or pressure on pelvic nerves
Reproductive symptoms like Infertility, recurrent abortion and preterm labour
The physical findings depend on the site, size and number. Submucosal myomas cause
symmetrical enlargement of the uterus while interstitial and subserosal ones cause
asymmetric enlargement of the uterus. The typical finding is a firm, irregular, non tender
mass attached to the uterus (moves with the cervix). Degenerative changes may give a
myoma varied consistencies.
Diagnosis is reached with history and physical examination in 95 % of cases. Additional
diagnostic modalities are ultrasound, hysterosalpingography and hysteroscopy.
5.5. Complications
Medical complications are anemia, uremia and rare reports of hypoglycemia and
polycythemia.
Gynecologic complications are torsion with gangrene, sarcomatous change, rupture of
surface vessel with intraperitoneal bleeding, chronic inversion and infection of delivered
myoma.
Obstetric complications are infertility, recurrent abortion, preterm labour, red degeneration,
malpresentation, uterine inertia, obstructed labour, postpartum hemorrhage and postpartum
necrosis.
5.6. Differential diagnosis
Pregnancy, adenomyosis, congenital malformation of the uterus, tuboovarian inflammatory
and neoplastic conditions and conditions that cause abnormal uterine bleeding
5.7. Management
There are two types of management for myomas.
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I. Conservative medical management
This is indicated for asymptomatic myomas of less than 12 weeks. Monitoring of the growth
of myoma by biannual pelvic examination and serial hemtocrite determination is done.
Where available, drugs like GnRh agonists are given to reduce the size and amount of
bleeding.
Another indication for medical management is red degeneration during pregnancy. The
treatment includes bed rest, analgesics and/or tocolytics. Laparatomy is only done if the
diagnosis is uncertain.
II. Surgical management
The indications are AUB leading to anemia, size of more than 14 weeks, and rapid increase
in size especially after menopause, hydronephrosis from myoma, infertility and recurrent
abortion resulting from myoma, uncertain nature of the tumor and severe pain from torsion.
The type of surgery is determined by the site and the desire for future fertility. It ranges from
conservative abdominal or vaginal nmyomectomy to total abdominal hysterectomy.
Hysterectomy is the definitive treatment of myomas.
6. Ovaries
I. Functional (physiologic) cysts
Follicular cysts result from failure of ovulation and are usually multiple with average size of
2 cm in diameter. Besides causing abnormal uterine bleeding (usually Oligomenorrhea with
menorrhagia), they rarely cause symptoms. They regress within 8 weeks.
Corpus luteum cyst is usually unilateral and rarely exceeds 4 cms in diameter. It causes
AUB in the form of oligomenorrhea. In most they are asymptomatic. Symptoms are related to
size and complications like hemorrhage, rupture and torsion. It resolves spontaneously within
8 weeks.
Theca luteum cyst is the least common functional cyst. It occurs in women with hydatidiform
mole and choriocarcinoma. It is usually bilateral with size ranging from microscopic size to
more than 15 cm in diameter. Symptoms are continued pregnancy symptoms and
occasionally pelvic and lower abdominal discomfort. It regresses after successful treatment
of the associated conditions.
II. Inflammatory lesions
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Tubo-ovarian complex or abscess and post vaginal hysterectomy ovarian abscess often
cause tender masses.
III. Hyperplasic lesions
Polycystic ovaries are found in Stein Leventhal syndrome (polycystic ovarian syndrome)
which manifests with obesity, oligomenorrhea /amenorrhea, hirsutism and infertility from
anovulation.
Others include leuteoma, serous inclusion cysts and endometrial cysts.
IV. Benign ovarian neoplasms
Depending on the histology the various types of benign ovarian neoplasms are epithelial
neoplasms, gonadal stromal tumors, nonintrinsic connective tissue tumor and germ cell
tumors. Epithelial tumors are the commonest benign ovarian tumors.
They usually occur during the reproductive age. Thecoma and Brenner tumors usually occur
in postmenopause. Size varies and may reach upto 30 cm in diameter in mucinous
cystadenoma. They usually present as pelvic or abdominal mass. Those secreting hormones
present with AUB.
Peculiar features of some benign ovarian tumors
“Pseudo mamma bodies” which are calcified concretion apparent on plain x-ray is seen in
serous cystadenoma.
“Abnormal sexual development” is seen in gonadoblastoma. Thus, gonadal removal after
puberty is recommended as there is a 25% risk of developing malignancy
“Meig’s syndrome”, is occurrence right side pleural effusion and ascitis with Brenner tumor.
Cystic teratoma (dermoid cyst) – contain sebaceous material, teeth; sweat glands, nervous
tissue and skin.
“Struma ovari” is a variant of cystic teratoma that has a thyroid tissue and manifests with
thyrotoxicosis
Surgical emergencies in benign ovarian tumors
Torsion of an ovarian cyst is more common in right ovary especially in pregnant and
children
Hemorrhage into the ovarian cyst
Rupture of and ovarian cyst may occur due to bleeding, torsion or trauma
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Management
Surgical removal is indicated for any of the following:
Premenarchal or postmenopausal palpable adenexal mass whether cystic or solid
Solid adenexal mass during reproductive age
Cystic adenexal mass that is more than 8 cm in diameter
Cystic adenexal mass of < 8 cm that persists for more than 8 weeks
Development of surgical emergencies
Observation with close follow up (clinical examination and serial ultrasound) is indicated for
cystic adenexal masses in reproductive age with size of < 8 cm in diameter.
7. Endometriosis
7.1. Definition
It is the presence of functioning endometrial glands and stroma outside their usual location in
the uterine cavity, resulting in pelvic adhesion. Common sites of endometriosis are ovaries,
tubes, uterosacral ligament, recto sigmoid colon, and bladder.
7.2. Epidemiology and pathogenesis
It affects women in their reproductive age years and regresses after menopause. The
different theories in its pathogenesis are
Retrograde menstrual flow
Metaplasia of coelomic epithelium
Vessel spread ( blood vessels or lymphatic vessels)
Genetic and immunologic influence
7.3. Clinical features
Symptoms are secondary dysmenorrhea, dysparunia, chronic pelvic pain; Infertility
Signs are fixed reteroverted uterus adenexal mass and indurations of the rectovaginal
septum. Diagnosis is made by pathologic examination of biopsied tissue obtained at
laparatomy/ laparoscopy.
7.4. Management
This is dictated by age, extent of the diseases, and desire for future fertility. The options are
medical treatment (nonsteroidal anti-inflammatory drugs, danazol, OCP, progestins and
GnRH agonists) and surgical treatment (conservative or radical surgery).
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MALIGNANT CONDITIONS OF THE FEMALE GENITAL TRACT
1. Vulvar cancer
It is an uncommon tumor accounting for 3- 5 % of primary genital tract cancers. It is a
disease of postmenopause with an average age of 60-65 years. Etiology is unknown STI
agents like human papilloma and herpes simple type 2 viruses are implicated. Conditions
that cause chronic vulvar irritation like diabetes mellitus, vulvar dystrophy and granulomatous
STIs (LGV) predispose to vulvar cancer.
More than 90% of primary vulvar cancer is squamous cell type. Others include melanoma,
basal cell carcinoma and verrucous carcinoma. More than 65% arise from the labia majora
and minora.
Squamous cell carcinoma usually starts as dysplasia of the vulvar skin in the third and fourth
decades of life. This usually manifests as pruritis or lump on the vulva. It spreads by direct
extension and by lymphatics to involve the inguinal, femoral and pelvic lymph nodes.
Despite its anatomic location late diagnosis is common mainly from reluctance of elderly
patients to seek medial advice and neglect of the health care worker to investigate vulvar
pruritis and lesions. The main symptoms are long standing pruritis, vulvar mass and ulcer.
Diagnosis is made by biopsy.
Note: All women with grossly suspicious vulvar lesion, confluent wart like mass, ulceration
that persists for more than 1 month should be referred for biopsy.
Surgery is the main stay of management with or with out adjuvant radiotherapy and
chemotherapy.
2. Vaginal cancer
Primary vaginal cancer is not common. The variants of primary vaginal cancer are
epidermoid (accounts for more than >75%), clear cell adenocarcinoma, sarcoma and
melanoma. It accounts for 2 – 4% of genital canal cancer. The mean age of occurrence is 55
years. Secondary vaginal cancer is the common form of cancer affecting the vagina. The
commonest primary site is the cervix followed by endometrium.
Clinical features are bloody vaginal discharge, ulceration or/and exophytic vaginal lesion,
pelvic pain and edema. Diagnosis is made by histologic examination of biopsied material
from the vaginal lesion.
Differential diagnosis includes granulomatous infections like LGV and genital tuberculosis,
chemical/ trauma induced ulcerations and endometriosis.
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Treatment options include surgery and radiation therapy.
3. Cervical cancer
3.1. Classification and staging
70-80% of cervical cancer is squamous cell type. It almost always (>90%) arises from the
transformation zone of the cervix at the squamocolumnar junction. It starts as dyplastic
change which eventually progresses to cervical cancer in situ and finally to invasive cancer.
This is a slow process which takes 7-10 years.
The next common type of cervical cancer is adenocarcinoma which arises from the
endocervical glands.
Cervical cancer spreads mainly by direct extension (vagina, uterus, parametrium, bladder
and rectum) and by lymphatic spread (pelvic lymph nodes, paraaortic nodes). Depending on
the progress it is staged clinically into four stages.
Stage O: Carcinoma in situ: Intraepithelial carcinoma
Stage I: Confined to the cervix
Stage- II: Extends beyond the cervix onto either the vagina or parametrium but not to the
lower 1/3 of the vagina and not to the pelvic wall.
Stage III: Extension either to the lower third of the vagina or to the pelvic wall.
Hydronephrosis or non-functioning kidney with no apparent cause necessitates
allocation to III B.
Stage IV: Extension beyond the true pelvis or involvement of mucosa of bladder or rectum
3.2. Premalignant lesions of the cervix (Cervical intraepithelial neoplasia)
Squamous cell carcinoma of the cervix develops from precursor lesions of the cervix called
cervical intraepithelial neoplasia (CIN), previously called cervical dysplasia. This is an
abnormal growth of cells in the transformation zone of the cervix that develops from the
squamocolumnar junction of the cervix.
Depending on the depth of the cervical epithelium, there are three types of CIN namely CIN1
(mild dysplasia), CIN2 (moderate dysplasia) and CIN3 (severe dysplasia or carcinoma in
situ).
Majority of CIN1 remain static or regress with only few progressing to CIN2. Significant
proportions (20-25%) of CIN2 progress to CIN3, the rest remain static or regress. CIN3 is
universally agreed to be a true cancer precursor with 30-70 % developing cervical cancer
over 10 years time.
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CIN lesions are characteristically symptomless. On naked eye examination, the cervix is
normal. Diagnosis is only made after biopsy. Detection needs special examinations. These
include
Pap smear (cervical exofoliative cytology), which is an ideal screening test for cervical
cancer. It should be done periodically (every 1 to3 years depending on the risk factors) in all
sexually active women.
Colposcopy
If the above tests show abnormal result biopsy is recommended.
Management includes ablation (destruction) of the transformation zone or conization of the
cervix or hysterectomy.
3.2. Etiology and risk factors
The exact cause of cervical cancer is unknown. But it is known to be a sex associated
disease, being rare in virgins. A number of sexually associated factors were implicated. Of
these, human papilloma virus types 16, 18 and31 are strongly associated with cervical
cancer. The risk factors for development of cervical cancer are
Sexual intercourse at an early age
Multiple sexual partners
High risk male partner (promiscuous partner, contact with cervical cancer patient)
Immunosuppression like HIV/AIDS
Smoking
Young age at first pregnancy
3.3. Epidemiology
Previously cervical cancer was the leading cancer of the genital cancer. But now its
incidence is decreasing because of early detection of preinvasive stage of the cancer. In
areas where regular screening is not available it is still a common gynecologic cancer.
Cervical cancer is the third most-common cancer world wide and the leading cause of death
among developing country women. An estimated 466,000 new cases of cervical cancer
occur annually among women world wide; about 80% occur in developing countries.
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3.4 .Clinical features and diagnosis
In early stages, cervical cancer is usually asymptomatic emphasizing the importance of
cytological screening to detect a cancer as early as possible.
Early symptoms include abnormal vaginal discharge which is offensive and watery and
abnormal uterine bleeding. Intermenustral bleeding post coital and contact bleeding and
postmenopausal bleeding are the usual forms of AUB. In advanced cases the patient
presents with pelvic and back pain and symptoms of uremia. Some times leg edema
develops.
In early stages the cervix appears normal. As the disease advances two types of appearance
may be seen depending on whether the lesion is endophytic or exophytic. In exophytic
lesions the cervix develops an ulcer and later cauliflower like growths into the vagina which
easily bleed to touch. In endophytic type the cervix is hard and nodular with variable surface
ulceration. In advanced cases there is infiltration of the vagina and necrosis of the tumor on
the cervix. Involvement of the rectum and the parametrial tissues is found on rectal
examination.
Diagnosis is made by pathologic examination of the tissue taken from the transformation
zone or from grossly abnormal sites on the cervix. Whenever a gross cervical lesion is
present, referral for a biopsy is indicated.
3.5. Complications
Uremia is the leading cause of death. Other complications are severe bleeding, sepsis and
pulmonary embolism.
3.6. Management
There are two options of management.
Surgical management - (total abdominal hysterectomy and pelvic lymphadenectomy) for
stages upto IIb
Radiotherapy – for all stages
3.7. Prevention
Invasive cancer of the cervix is considered a preventable cancer because it has a long
preinvasive state, a sensitive screening method to detect preinvasive stages and effective
the treatment for pre-invasive lesions.
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Papanicoaus smear is a cervical cytology study that should be done in all sexually active
women every 1-3 years. It is an ideal screening test for detection of precancerous stage of
cervical cancer.
4. Endometrial cancer
4.1. Classification and staging
Endometrial cancer is an adenocarcinoma of endometrial glands. There are different
histologic variants with different impact on the prognosis. Some of these variants are
endometriod type carcinoma, adenosquamous carcinoma, clear cell carcinoma, papillary
carcinoma and secretory adenocarcinoma.
It spreads mainly by direct contagious and lymphatic routes. In late cases haematogenous
spread occurs. Unlike cervical cancer, endometrial cancer is staged surgically.
4.2. Etiology and risk factors
Most develop in hyperestrogenic states with unopposed estrogen action without cyclic
influence of progesterone. Antecedent endometrial hyperplasia is found in most endometrial
cancers. The risk factors are
Age of 55- 65 years (postmenopausal), rarely occurs before 40 years
Early menarche, delayed menopause
Infertile or history of repeated abortions, nulliparity
Obesity , hypertension, diabetes and middle class life style
Hyperestrogenic states like chronic anovulation (Stein Leventhal Syndrome), estrogen
secreting tumors, exogenous estrogen use
4.3. Epidemiology
The incidence is 12-15 /100000 women and increasing over the years. The peak age is 60-
70 years. It is mainly a disease of post menopause which accounts for 75% of the cases.
15% occurs in the perimenopausal period and the rest in the premenopausal time.
4.4. Clinical features and diagnosis
The principal symptom is abnormal uterine bleeding. It is usually of postmenopausal type
with scanty, small and recurrent bleeding. In the premenopausal period it may take the form
of menorrhagia, polymenorrhea and intermenustral bleeding. The second common symptom
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is abnormal vaginal discharge which is usually offensive. In advanced disease pelvic
pressure from hematometra/ pyometra, weight loss and debility occurs.
The usual finding on physical examination is moderately enlarged uterus.
Diagnosis is reached by histopathological examination of endometrial tissue. This can be
done by simple endometrial biopsy/ curettage/aspirate or commonly by fractional curettage
which is considered to be the gold standard for diagnosis..
Note: All women with abnormal uterine bleeding in the perimenopausal and
postmenopausal period should be referred for diagnostic curettage and surgical
staging.
4.5. Management
The definitive management is surgery (total abdominal hysterectomy + bilateral
saphingeophorectomy + pelvic lymphadenectomy) supplemented by radiation and/ or
chemotherapy.
4.6. Complications
These include hematometra, pyometra and perforation / rupture of uterus.
5. Ovarian cancer
5.1. Classification and staging
Ovarian cancer is classified by the histologic types. Epithelial tumors are the commonest
accounting for 90% of all ovarian cancers. The remaining 10 % include germ cell, gonadal
stromal, nongonadal stromal and unclassified tumors.
Ovarian cancer spreads mainly by transperitoneal route and by direct extension. It also uses
lymphatic and in advanced cases haematogenous routes. Staging is done surgically during
laparatomy.
5.2. Epidemiology and risk factors
Risk for epithelial cancers increases upto 80 years of age. It accounts for 4% of cancers in
women and contributes for 40% of deaths related to gynecologic cancers. It is called the
silent killer because of nonspecific symptoms and difficulty in accessing the ovaries by
physical examination and absence of reliable screening test for detection of early lesions.
Some of the risk factors for epithelial ovarian cancer are high fat diet, early age at menarche,
late menopause, and history of premenstrual syndrome, nulliparity, celibacy and repeated
abortions.
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5.3. Clinical features
Symptoms are non specific and are usually absent in early stages. These include nausea,
vomiting, bloating abdominal fullness constipation and flatulence. Hormone secreting tumors
are associated with AUB. Weight loss is a late manifestation.
In early stages there will not be any abnormal physical finding but later one may find ascitis,
pelvic or abdominal mass, hepatomegally pleural effusion and lymphadenopathy (inguinal or
supraclavicular).
Definitive diagnosis is made by histopathology of a biopsy made during laparatomy.
5.4. Management
Surgery (total abdominal hysterectomy, bilateral saphingeophorectomy, omentectomy,
appendectomy along with resection of grossly visible lesions) supplemented by
chemotherapy and or radiotherapy
Review questions
1. Discuss the degenerative changes and clinical features of myoma.
2. Discuss the risk factors, complications and prevention of cervical cancer.
3. List the indications for surgery for an adenexal mass.
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CHAPTER 31
UTEROVAGINAL PROLAPSE AND URINARY INCONTINENCE
Learning objectives
To discuss the anatomic supports of the uterus and vagina
To classify uterovaginal prolapse
To discuss the causes of uterovaginal prolapse
To discuss the diagnosis and management of uterovaginal prolapse
To list the different types of urinary incontinence and their clinical features
To discuss the different tests used in the diagnosis of urinary incontinence
1. UTEROVAGINAL PROLAPSE
Anatomic supports of the uterus and vagina
A condensation of the parietal endopelvic fascia running from the back of the symphysis
pubis to the ischial spines provides the origin of the levator ani muscle. The parietal
endopelvic fascia over the levator ani is condensed in certain areas to forming ligaments that
are very important in supporting the uterus. Of these ligaments the cardinal ligament or
Mackenrodt’s ligament is the most important one. It runs from the lateral sides of the cervix
to the lateral pelvic wall. The others are uterosacral ligament and pubocervical fascia.
In addition to the facial supports of the cervix, the uterus receives from the round ligaments,
which keep it anteverted and the infundibulopelvic ligaments. Another significant aspect to
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the anatomic support of the uterus is its anteverted and anteflexed position in relation to axis
of the vagina.
The levator ani and the perineal muscles along with the rectovaginal septum provide the
most important muscular support for the vagina.
Definition and types
Uterovaginal prolapse is the downward descent of the uterus and the vagina from their
normal pelvic positions.
Fundamentally, there are two types of genital prolapse
I. Vaginal prolapse
Anterior vaginal wall prolapse – may exist in the form of cystocele (herniation of the bladder
base into the upper vagina), urethrocele (herniation of the posterior wall of urethra into the
lower part of the vagina) or cystourethrocele (herniation of the entire anterior vaginal wall).
Posterior vaginal wall prolapse – can present as a rectocele (herniation of the rectum into
the vagina, usually involving the lower one half or two thirds of the posterior vaginal wall)
and/or enterocele (herniation of a peritoneal sac of Pouch of Douglas into the upper part of
the posterior vaginal wall that may contain loops of small bowel).
Vault prolapse: refers to a herniation of a peritoneal sac at the vaginal vault after abdominal
or vaginal hysterectomy
II. Uterovaginal prolapse
The uterine component of the uterovaginal prolapse is measured in relation to the degree of
prolapse of the cervix below the level of the ischial spines (the normal station of the cervix in
the pelvis)
First degree prolapse – refers to descent of the cervix below the ischial spines as far as, but
not beyond, the introitus
Second degree prolapse – descent of the cervix (but not the entire uterus) beyond the
introitus
Third degree prolapse (procidentia) is herniation of the entire cervix and uterus beyond the
introitus.
Etiology
The causes of uterovaginal prolapse are
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Childbirth related trauma to the pelvic support and improperly repaired genital tract tears
Climacteric related atrophy of the pelvic supports
Chronic increase in intra abdominal pressure from chronic cough and constipation
Congenital weakness of the pelvic supports
Neurologic problems affecting the pelvic musculature
Clinical Features
The symptoms of genital prolapse could be general or specific. The general symptoms are
Painless mass bulging through the introitus which is prominent when standing or straining
Pelvic pressure or bearing down sensation in the pelvis or sensation of something coming
down or dragging discomfort and low back pain
The specific symptoms are
For anterior vaginal wall prolapse: stress incontinence, symptoms of urinary tract infection,
sense of incomplete emptying and urinary retention
For posterior vaginal wall prolapse: constipation, rectal fullness, difficulty in emptying the
bowel, sense of incomplete emptying which necessitates splinting or digital removal
For enterocele: usually nonspecific symptoms resulting from traction of the abdominal
viscera
For uterine prolapse: abnormal uterine bleeding, abnormal vaginal discharge
The physical findings are
For anterior vaginal wall prolapse: soft, reducible mass bulging into the anterior vagina and
distending the vaginal introitus (best demonstrated by means of Sim’s specula with the
patient in left lateral position). With straining or coughing it bulges more and may be
associated with stress incontinence.
For rectocele: soft, thin walled mass projecting into the posterior vaginal wall. On rectal
examination, the rectovaginal septum projects well into the vagina and there is anterior
sacculation of the rectum into the vagina.
For enterocele: rectovaginal examination, especially with the patient standing, reveals a
reducible thickness or bulging of the upper recto vaginal septum. Occasionally loops of bowel
may be felt in the mass.
For uterine prolapse: Almost always there is an associated anterior and posterior
vaginal wall prolapse. In addition, visualization or palpation of the cervix with or
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without the patient straining and palpation of the uterus grades the degree of uterine
prolapse. In long standing cases decubitus ulcer and thickened cervical/ vaginal
epithelium is seen.
Complications
Keratinization of the vagina and cervix
Decubitus ulcer on the cervix
Urinary tract infection and urinary obstruction (angulation of the urethra or constriction
of the ureters in procidentia)
Incarceration of the prolapse
Sexual dysfunction
Management
I. Medical measures:
Small or moderate sized cystocele and rectocele and first degree uterovaginal prolapse
requires reassurance, explanation and pelvic exercise (Kegel’s exercise) for 6-12 months.
Other medical measures are vaginal pessaries, estrogens for postmenopausal women.
Note: Kegel’s exercise is done by repeatedly contracting the pubococcygeus muscle as if
one is trying to stop urination (150 – 200 x /day)
II. Surgical measures
For cystocele: anterior colporrhaphy
For rectocele: poteriorcolpoperineorraphy
For uterovaginal prolapse: The standard surgery is vaginal hysterectomy combined with
anterior colporrhaphy and posterior colpoperineorraphy. Other options are Manchester
operation (combines anterior colporrhaphy, cervical amputation, posterior
colpoperineorraphy and suturing of cardinal ligaments in front of the cervix) and Lefort’s
partial colpocleisis (partial suturing of anterior and posterior vaginal walls together).
Prevention
Encouraging postnatal perineal exercises
Proper suturing of perineal and vaginal lacerations with proper anatomic restoration
Avoidance of excessive fundal pressure during delivery
Treatment of chronic cough and constipation
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2. URINARY INCONTINENCE
Definition and classification
Urinary incontinence is an involuntary leakage of urine due to involuntary reversal of the
pressure gradient between the bladder and urethra. The various types of urinary
incontinence are
Genuine stress incontinence
Motor urge incontinence (unstable bladder)
Sensory urge incontinence
Overflow incontinence
Bypass incontinence
Psychogenic incontinence
Etiology
When the urinary tract is intact, continence is maintained as long as the pressure closing the
urethra is greater than the intravesical pressure. When this pressure gradient is reversed,
urine passes to the urethra. This occurs in voluntary micturition due to the urethral relaxation
and detrusor muscle contraction.
Urinary incontinence may be due to any of the following, alone or in combination
Lowered urethral pressure (momentary or continuous)
Detrusor contraction
Greater transmission of intraabdominal pressure to the bladder than to the urethra
Passive increase in intravesical pressure due to distension beyond the elastic units of the
bladder
Bypassing of the continence mechanism
Tests and investigations
Urinary stress test is done by instilling 300 ml of saline in the bladder and the patient
performs Valselva maneuver eight to ten times while standing with feet spread as wide as
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the shoulders and the perineum is inspected for leakage of urine. It provides gross
quantization of degree of incontinence. In 20% false negative results are found.
Pad test is done when the stress test is negative (no urine leakage). In this procedure the
patient wears preweighed sanitary napkin, does some exercise and then the pad will be
reweighed to determine how much urine has been lost. It is used to assess degree of
incontinence.
Cotton – tipped applicator ( Q-tip) test - assesses the degree of bladder or urethral
descent during straining by measuring the angle formed by the applicator stick and an
imaginary line parallel to the floor while patient is in lithotomy position and doing Valselva
maneuver. An angle of < 15O both during rest and the Valselva maneuver shows good
anatomic support. An angle of > 30O during the Valselva maneuver shows poor anatomic
support. An angle of 15 – 30O is considered inconclusive.
Bonney test- assesses support of proximal urethra. It is performed in a woman with stress
incontinence by putting the index and middle fingers in the vagina, lifting the bladder base
towards the pubic bone and asking the woman to strain or cough. If there is no incontinence
then the diagnosis of poor urethral support is made. If there is incontinence then other
causes of stress incontinence are looked for.
Dye (cotton ball) test- this is a test to detect small vesicovaginal fistulas and differentiate
vesicovaginal fistula from other types of urinary fistulas (urethero and ureterovaginal fistula).
It is done by putting three cotton balls into the vagina and instilling diluted methylene blue
into the urinary bladder through a bladder catheter. If the dye stains the upper cotton balls
then the diagnosis of vesicovaginal fistula is made. If there is no staining with the dye then
consider ureterovaginal fistula as a cause. are
Urine analysis and culture
cystoscopy/ urethroscopy
1. Genuine Stress incontinence (GSI)
GSI is the involuntary loss of urine through the urethra occurring simultaneously with an
increase in intraabdominal pressure but in the absence of detrusor muscle contraction.
Pathophysiology
Normally at rest the intraurethral pressure is greater than the intravesical pressure. The
pressure difference or urethral closure pressure represents the margin of continence.
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Therefore, if the resting intravesical pressure plus any increase in pressure generated during
stressful activities (coughing, exercise) exceeds the intraurethral pressure at rest plus any
increase in urethral pressure generated during the activities, the urethral closure pressure
will decrease to zero, and genuine stress incontinence will result.
Etiology
Two possible causes exist
Anatomic descent of the proximal urethra below its normal intraabdominal position during
stressful activities, altering the vesicourethral angle: This occurs in anterior vaginal wall
prolapse, especially with urethrocele.
Failure of neuromuscular mechanisms that increase intraurethral pressure which result in the
dysfunction of the extrinsic or intrinsic urethral sphincter.
Clinical Features and diagnosis
Classic symptom is involuntary loss of urine which occurs simultaneously with stressful
activities like coughing, sneezing and laughing. It stops as soon as the stressful act is over.
Examination will usually show variable degree of cystourethrocele in 75 % of the cases. In
cases of anatomic descent of the urethra, poor support of urethra can be demonstrated by
clinical tests like Q-tip test which is abnormal in 95% of GSI.
Criteria for diagnosis of genuine stress incontinence are
Normal neurologic examination
Poor anatomic support (Q – tip test, X-ray or urethroscopy)
Demonstrable leakage with stress (stress or pad test)
Normal urine analysis, negative urine culture
Normal cystometrogram or urethrocystometry
Management
I. Medical measures
For poor anatomic support: Kegel’s exercise, estrogen for postmenopausal
For intrinsic sphincteric defect: a adrenergic agonists
II. Surgical measures for severe cases either by abdominal or vaginal approaches
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2. Motor urge incontinence (detrusor instability, unstable bladder)
This Is the result of involuntary uninhibited detrusor muscle contractions in most cases
idiopathic in origin. It may be associated with cystitis. In most it is idiopathic. It is the second
most common cause of urinary incontinence. Because of its unpredictability and loss of large
volumes of urine, it has greater detrimental effect on patients than GSI.
Pathophysiology
Normally increasing detrusor contractions occur when the bladder contains more than the
cystometric capacity (the bladder volume that can be tolerated in the awake, unanesthetized
state). Micturition occurs because of the increase in the intravesical pressure and along with
simultaneous voluntary relaxation of the external urethral sphincter. This process can be
inhibited voluntarily at any time.
In unstable bladder uninhibited detrusor contractions typically occur spontaneously or upon
provocation (as coughing, exercise, tactile or auditory stimuli) at bladder volumes below
normal resulting in incontinence.
Clinical Features and diagnosis
Symptoms are usually multiple. Patients usually have a strong urge for urination moments
before incontinence. If associated with stressful activities, incontinence occurs seconds after
the stress has started and will continue after the stressful activity is over, despite the patients
effort to stop it. Symptoms of urinary tract infection may be present. The physical
examination may be normal. Anatomic support of the bladder and urethra may be good or
poor. Neurologic signs are typically absent.
Diagnosis is based on finding delayed urinary leakage or continuous heavy flow despite the
patient’s effort to stop during the urinary stress test and simultaneous urethrocystometry
confirms the diagnosis.
Management
I. Medications
Anticholinergic agents are the most effective
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Others include smooth muscle antispasmodics, calcium channel blockers and
prostaglandin synthase inhibitors
II. Behavior modification: bladder retraining and psychotherapy
III. Surgery is the last resort in the management: denervation, cystoplasty and urinary
diversion are the procedures
3. Sensory Urge Incontinence
It is leakage of urine (in association with great urgency) that occurs in a stable bladder
without excessive descent of the urethra or bladder.
It is associated with bladder irritation as it occurs in cystitis, bladder stone or neoplasia.
Psychological factors may also play a role. This stimulates the afferent arc of micturition
reflex resulting in strong urgency to micturate. has the ability to inhibit detrusor contraction
and does so when instructed showing that her bladder is stable.
Clinical Features and diagnosis
Incontinence is associated with frequency, urgency, dysuria and /or hematuria. Urine
analysis and culture show urinary tract infection. Urethroscopy and cystoscopy are important
to diagnose underlying pathologies like calculi and neoplasms. Cystometric findings are
usually normal.
Management
Treatment of infections
Treatment of the specific underlying cause
4. Overflow Incontinence
Etiology
Urinary retention and subsequent overflow incontinence can be caused by
Lower motor neuropathies and diabetes
Obstructive causes in postoperative period or by pelvic masses
Pharmacologic causes: ganglionic blocking agents, anticholinergics
Treatment
Treatment of the underlying cause
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Medical management directed towards reducing urethral closure pressure and increasing
detrusor contractility
5. Bypass Incontinence
Urinary leakage occurs as a result of bypassing of the normal anatomic urethral continence
mechanism. It is characterized by continuous leakage of urine. Commonest cause is urinary
fistula. Others are ectopic ureter (leakage starts from early age) and urethral diverticula’s
(leakage occurs with change of position minutes or hours after urination).
Treatment is usually surgical depending on the specific cause and the prognosis is generally
good.
6. Urinary Fistula
Definition
It is a direct communication between the urinary and genital tracts. It could be vesicovaginal
(commonest between the vagina and the bladder), ureterovaginal (between the ureters and
rthe vagina), urethrovaginal (between the vagina and the urethra) and vesicouterine
(between the uterus and the bladder).
Etiology
Obstructed labor is the commonest cause of urinary fistulas. The other causes are advanced
genital cancers (cervix, vagina, and endometrium), trauma (rape, ghorning accident),
radiotherapy and lymphogranuloma venereum.
Clinical features
Continuous leakage of urine per vagina is the hallmark of urinary fistulas. Speculum and
digital examination may identify hole in the anterior vaginal wall with urine coming through.
Small ones can be identified by doing dye test or cystoscopy or intravenous pylogram.
Management
I. Fistulas following obstructed labour
Small ones may close spontaneously. In these cases, continuous catheter drainage (bladder
or ureteric) should be tried for three weeks. If it persists then surgical closure after three
months should be planned. This will allow adequate healing of the surrounding ischemic
tissue. Ample fluid intake during this time will prevent calculi formation at the fistula site.
Method of repair depends on position of fistula, size of the defect and degree of fixity.
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Note: Unless the fistula is very small, women with repaired fistulas should be
delivered by elective caesarian section.
II. Other types of fistulas
Surgical closure is the method of management. Success depends on the cause.
7. Psychogenic Incontinence
It can take any form of the incontinences discussed above. It is commonly diagnosed in
patients with significant psychologic or psychiatric disorders.
Review questions
1. Describe the classification, causes and diagnosis of uterovaginal prolapse.
2. List the complications of uterovaginal prolapse.
3. List the different types of urinary incontinence.
4. Describe the different tests used in the diagnosis of urinary incontinence.
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References
1. DeCherney AH, Pernoll ML Current. Obstetrics and Gynecologic diagnosis and
treatment, 8th edition.
2. Larry J. Copeland, Text Book of Gynecology
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3. Lawson J. B, Stewart D. B, Obstetrics and Gynecology in the Tropics and developing
countries
4. Scott JR, Danforth’s text book of Gynecology & Obstetrics, 1996
5. Novak’s text of Obstetrics & Gynecology, 10th edition, 1981.
6. Department of Obstetric and Gynecology, The management of infertile couple protocol.
AAA, Faculty of Medicine, 2000
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ANNEX 1
EPIDEMIOLOGY OF OBSTETRICS AND GYNECOLOGIC PROBLEMS
1. OBSTETRIC BASIC STATISTICS
1. Birth - Complete expulsion of a fetus from the mother
2. Live birth - Any fetus that is born with any sign of life regardless of fetal weight or
gestational age.
3. Still birth - The birth of a fetus with no sign of life (WHO weight greater than 500grams or
greater than 20 weeks of gestation and in Ethiopian context weight greater than or equal to
1000 grams and greater than 28 weeks).
4. Still birth rate- Number of stillbirths /1000 live births.
5. Neonatal mortality rate - number of live born infant death within first 28 days per
1,000 live births
· Early neonatal death – Live born infant deaths within first 7 days of life
· Late neonatal death- Live born infant deaths within first 28 days of life excluding the
first 7 days of life
· Neonatal period I - From birth through 23 hours and 59 minutes.
· Neonatal period II- 24 hours through 6 days, 23 hours and 59 minutes
· Neonatal period III- from 7 days through 27 days, 23 hours and 59 minutes
6. Perinatal mortality rate (PMR) - Number of still births and number of neonatal death in
1st 7 days of life per 1000 live births.
· In developing countries, 3 million neonates die in first week after delivery and 4 million
are still births.
· PMR in developing countries ranges from 40 to 60 /1000 live births, but it is between 6 to
10 /1000 live births in developed countries.
· Major causes of perinatal death are mechanical trauma during delivery, hypertension in
pregnancy, antepartum hemorrhage, fetal malformations, low birth weight and Infections.
7. Fertility rate - Number of live births per 1000 women between age of 15 and 44 years of
age.
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8. Reproductive mortality: - Death due to direct result of pregnancy or use of contraceptive
per 1000 women
9. Maternal mortality - Death of a woman while pregnant or within 42 days of termination of
pregnancy irrespective of the site & duration of pregnancy, from any acutely related to or
aggravated by the pregnancy or its management but not from accidental or incidental cause.
10. Maternal mortality rate - Number of maternal deaths due to reproductive process
per100, 000 live births
· 500,000 maternal deaths occur each year world wide
· 99% of maternal death occurs in developing countries
· In Africa maternal death is 630/100,000 live births
· East Africa maternal death is 680/100,000 live births
· Lifetime risk of maternal death in Africa is 1 in 21
According to the etiology maternal deaths are subdivided into:
Direct maternal death: Maternal death is directly attributable to obstetric causes or the
quality of obstetric care.
Indirect maternal death: Maternal death is attributable to a concomitant disease &
conditions aggravated by the pregnancy.
Non maternal death: Maternal death due to accidents & not related to pregnancy.
Major causes of maternal death in the developing countries include
· Hemorrhage 25%
· Infection (sepsis)15%
· Unsafe abortion 13%
· Hypertensive disorders 12%
· Obstructed labor 8%
· Indirect causes 19%
· Others 8%
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2. DEMOGRAPHIC STATISTICS
1. Crude birth rate (CBR) = Number of total births per 1,000 total population per year at
midyear.
2 Crude death rate (CDR) = Number of death per 1000 total population per year at mid year.
3. Crude rate of natural increase (CRNI) = CBR-CDR per1000 population per year
4. Population growth rate (PGR) = CRNI + the sum of the migration of people in and out of
the population.
5. Life expectancy (LE) = Average number of years of life remaining in individual at a
specific age.
Population Trend
· World population growth increase at a rate of 2% per year and doubles every 35 years.
· World population 1980 was 4.4 billion; at 2000 it was 6.2 billion. At the time of Christ, it
was about 250 million.
· If the trend continues, there may be 12 billion people in the world by the year 2035.
3. HEALTH INDICATORS FOR THE STATUS OF WOMEN IN ETHIOPIA
· Fertility rate 6.2
· Antenatal care utilization 20%
· Assisted deliveries by trained health worker 14%
· Family planning coverage less than 10%
· MMR= Average 500-700 /100,000
4. EXPOSURE & DISEASE IN GYNECOLOGY
Exposure to some factors may cause female genital organ disease.
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4.1. Exposure
4.1.1. Reproductive events
Age at menarche, character of menstrual cycle, gravidity and age of menopause have
impact on endometriosis, myoma, heart disease, and osteoporosis, cancer of breast,
endometrium and ovary.
4.1.2. Contraceptive and sterilization
Barrier methods are protective of pelvic inflammatory disease, tubal infertility, ectopic
pregnancy and cervical cancer.
Intrauterine devices - increases pelvic inflammatory disease, tubal infertility and ectopic
pregnancy
Oral contraceptives- increase the risk of thromboembolism, hypertension, myocardial
infarction and liver adenoma. They are protective against benign breast disease, ovarian
cancer and pelvic inflammatory disease
Sterilization- induces early menopause and protective for ovarian cancer.
4.1.3. Menopausal hormones
Increase endometrial cancer, protective effect on heart disease, osteoporosis and
Alzheimer disease.
4.1.4. Sexually transmitted infections
Predispose for HIV, syphilis, pelvic inflammatory disease, chlamydia and gonorrhea.
4.1.5. Life style
Smoking – increase heart and lung disease, tubal infertility, ectopic pregnancy, cervical
cancer and early menopause.
Alcohol- Decrease cardiovascular disease, risk of breast cancer increased, Increases
circulating estrogen
Exercise and nutrition : lean athelets and anorexia nervosa cause amenorrhea, obesity
causes menstrual difficulty and endometrial cancer
Talc use- increases risk for ovarian cancer
4.2. Disease
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· Mortality caused by cancer in decreasing order: lung cancer, breast, colorectal,
pancreas and ovary.
· Incidence of gynecologic cancer in decreasing order: cervical, endometrial and
ovarian cancer, but mortality is higher in ovarian tumor.
· Incidence of benign gynecologic conditions varies from place to place: pelvic
inflammatory disease, benign ovarian cyst, endometriosis, myoma, ectopic
pregnancy.
ANNEX 2
THE PARTOGRAPH
The partograph is a tool to assess and interpret the progress of labour. Its central feature
is graphic record of cervical dilatation but descent of the fetal head and uterine activity are
also indicators of progress of labour. It also detects other problems developing in the
mother and the fetus.
Advantages include
It gives comprehensive view of all major events of labour
It allows early detection and management of abnormal labour patterns
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It simplifies handover to other health professionals
It saves time and is more efficient
It is simple (only symbols and letters are used) and skill in its use is quickly attained.
It helps in research and teaching
Parts
The WHO model partograph has three parts that assess different parameters.
I. Labor progress
Cervicograph: Four hourly digital pelvic examination is done and cervical dilatation is plotted
by mark X on the graph whose vertical arm shows the cervical dilatation in centimeters and
horizontal arm shows the time. The graph has a latent phase which has 8 hours limit and an
active phase which takes the rest of the graph to the right of the latent phase. A vertical
line drawn at 8 hours mark separates the two. A horizontal line drawn at 3 centimeters of
cervical dilatation separates the latent and active phases. On the active phase there are two
parallel diagonal lines set at four hours apart. They are named the alert line (the one found
on the left side) and the action line. Labour is said to be progressing normally if the cervical
dilatation curve stays to the left of the alert line. Strict observation (in a health center
preparation for referral) is indicated if the curve crosses the alert line. Action in the form of
augmentation or caesarian section or referral for these measures must be done if the curve
crosses the action line.
Descent of the fetal head is assessed by abdominal examination in fifths and plotted on the
cervicograph with a mark 0.
Uterine contraction is assessed by abdominal palpation for 10 minutes every 30 minutes.
The number of uterine contractions in 10 minutes and their average duration is then plotted
on the squares provided. Corresponding number of squares are shaded to indicate the
number of uterine contractions. The average duration of contraction is plotted by filling the
squares with different shades. If the duration is less than 20 seconds the squares are filled
with dots. If between 20- 40 seconds fill with striped lines. If greater than 40 seconds
completely shading of the squares is done.
II. Fetal condition
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Fetal heart rate is counted by intermittent auscultation every 15 minutes. It is recorded in by
writing in numbers in the square provided.
Molding of the fetal head is obtained during pelvic examination. According to its degree it is
given different codes. If the bones of are separate it is recorded as 0. If they are touching
each other but not overlapping it is recorded as +. If they are overlapping but can be
separated by digital pressure it is given ++. If they are overlapping and can not be separated
digitally it is given +++.
Color of the liquor is observed during pelvic examination. The letter I is used for intact
(unruptured) membranes. The letter C is used for ruptured membranes with clear liquor and
letter M if the liquor is muconium stained.
III. Maternal condition
Blood pressure is measured every 4 hours or more frequently if there is hypertension. It is
on the vertical lines using to v indicate the systolic pressure and ^ to indicate the diastolic
pressure.
Pulse rate and temperature are measured every 1-2 hours and the number is entered into
the square provided.
Urine volume, dipstick (for glucose and ketone) and microscopy is performed and recorded
in space provided.
Drugs given to the mother along with the doses is also recorded.
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