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"MKS NOTEs IN Ob MKS NOTEs IN Ob MKS NOTEs IN Ob MKS NOTEs IN Ob/ // /Gyn Gyn Gyn Gyn "
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Contributors

Ayah M Boudal, medical student 2008
Development and Congenital Abnormalities of the Reproductive System, The anatomy of
female genital tract, Ovulation, Fertilization, Implantation and the Placenta.

Badr Rajb, medical student 2008
The menstrual cycle.

Dalal Al-Omar, medical student 2008
Miscarriage (Abortion), Pap smear.

Elham Algethami, medical student 2008
Renal disease in pregnancy.

Faisal Al-Gaows, medical student 2008
Infertility.

Jameel Khalid Rasheedi (Dr.JKR), medical student 2008
Amenorrhea.

Mohammad Bokhary, medical student 2008
Normal Labor, Diabetes Mellitus during Pregnancy.

Nedaa bhkali, medical student 2008
Development and Congenital Abnormalities of the Reproductive System, The anatomy of
female genital tract, Ovulation, Fertilization, Implantation and the Placenta.

Roa'a Mursi, medical student 2008
Premature Rupture of Membranes, Preterm Labour (PTL).

Salman Jan, medical student 2008
Ob/Gyne Instruments, Gestational Trophoblastic Disease-GTD.

Sameerah Albugami, medical student 2008
Bleeding in 3
rd
Trimester (Antepartum Hemorrhage).

Wafaa Al-Ahmadi, medical student 2008
Abnormal Labor & Delivery, Intrauterine Fetal Death (IUFD), Intrauterine Growth Restriction
(IUGR),Pelvic Mass, Pelvic pain, Ovarian cancer, Cervical cancer, Induction & augmentation of
labour, Postpartum Hemorrhage (PPH).



Design and production:
Jameel Khalid Rasheedi (Dr.JKR)
Suheab Abdulhamaid Maghrabi

With participate of
Iman Hani
C o n t e n ts
G Y N E C O L O G Y
The anatomy of female genital tract .1
Development and Congenital Abnormalities of the Reproductive System ..8
The menstrual cycle.12
-Premenstrual Syndrome (PMS).16
Pelvic Mass...17
Pelvic pain24
Amenorrhea .29
Infertility ..37
Ovarian cancer..41
Cervical cancer.46
Gestational Trophoblastic Disease-GTD.51

O B S T E T R I C S
Ovulation, Fertilization, Implantation and the Placenta..57
Diabetes Mellitus during Pregnancy....67
Renal disease in pregnancy...72
Bleeding in 3rd Trimester (Antepartum Hemorrhage).. ... 75
- Placenta previa 75
- Abruptio placenta 76
- Vasa previa..80
Miscarriage (Abortion) 81
Intrauterine Fetal Death (IUFD).83
Intrauterine Growth Restriction (IUGR)86
Normal Labor & Dystocia91
Induction & augmentation of labour96
Abnormal Labor & Delivery .100
- Labor Dystocia.100
- Malpresentation...102
-- breech: . .102
--- External cephalic version (ECV) ..102
-- Transverse (shoulder presentation) or oblique ...103
-- Other malpresentation103
- Intrapartum complications:..104
-- Shoulder dystocia104
-- Cord prolapsed 105
-- Other congenital neurological birth injuries 105
-- Intracranial hemorrhage ..105
Preterm Labour (PTL)106
Premature Rupture of Membranes.111
Postpartum Hemorrhage (PPH)115
Pap smear118
Ob/Gyne Instruments121
The anatomy of Female Genital Tract

Prepared by: Ayah M. Boudal ,and Nedaa bhkali
Source: Tareg arab sheets



The perineum is the inferior boundary of floor of the pelvis .
Bounded : Levator ani (superior)
Skin of thighs (inferior)
Extends : Symphyisis pubis and inferior borders of pubic bones (anteriorly)
Limited by ischial tuberosities , sacrotuberous ligaments and coccyx (posteriorly)
- The superficial and deep transverse perineal muscles cross the pelvic outlet between
the ischial tuberosies , and oin at the perineal body.
- They divide the outlet into urogenital triangle anteriorly and anal triangle posteriorly .
Urogenital triangle :
- Anterior to the anal triangle
- Bounded by the symphyisis and pubic rami .

Anal triangle :
- Posterior to the urogenital triangle
- Bounded by the ischial tuberosities , sacrotuberous ligaments and coccyx
The perineal body lies between the anal canal and the lower third of the vagina .






Urogenital diaphragm : pierced by the following structures :
- Vagina - Internal pudendal vessels
- Urethra - Dorsal nerve of clitoris - Artery of bulb

Inferior surface : Crura of clitoris Superficial
Perineal muscles
Vestibular bulbs
Bartholin glands
The transverse perineal muscles (profunda and superficialis ) form the perineal body. This is important
because often it is cut to facilitate birth.

Types of pelvis :
1- Gynecoid : t.d > ap.d , round inlet, classical female pelvis 60%
2- Android : typical male < 30%
3- Anthropoid : < 20% ap >> t.d (oval)
4- Platy pelloid : 3% ap<< t.d (oval)

Nerves of the pelvis :

Branches of the sacral plexus, which lies on the posterior pelvis wall in front of piriformis muscle.
- Branches to the pelvic muscles, viscera, perineum :
Pudendal nerve (S2,S3,S4) : external anal sphincter, mucous membrane of lower half anal
canal , perianal skin, clitoris , labii majora and minora .
Nerves to piriformis
Pelvic splanchnic nerves (S2,S3,S4) : sacral part parasymp
system
Perforating cutaneous nerve : supplies skin of lower medial
buttocks

- Branches to lower limb via greater sciatic foramen :
Sciac nerve (L4,L5,S1,S2,S3)
Superior gluteal nerve : gluteus medius , minimus and
fasciae lata
Inferior gluteal nerve : supplies gluteus maximus
Nerve to quadrates femoris
Nerve to obturator internus muscle
Posterior cutaneous nerve of the thigh

Blood supply of the pelvic organs :

Ovarian , internal iliac , and superior rectal arteries and veins

Lymphatic drainage :
Vulva and lower vagina : iguino-femoral lymph nodes to the external iliac nodes
Cervix : (Via the cardinal ligaments) pelvic nodes to the common iliac and para-aortic nodes
Endometrium : Via the broad ligament to pelvic and para-aortic chains
Ovaries: Via the infundibulo-pelvic ligaments to pelvic and aortic nodes






- Known as the vulva or pudenda
- Innervated by pudendal nerve
- Anterior to the vulva,innervations by ilioinguinal and genitofemoral nerves


Consists:
Mons pubis (target of testosterone, site of pubic hair )
Labii (majora) rich blood supply , hairy
Labia (minora) , posterior folds attach inferior surface clitoris , ant form prepuce , hairless
Clitoris (in front of urethra , consists glands,body,crura)
Bartholin`s gland (columnar epithelium) . Cyst forms if duct blocked
Furchette (where the minora attach ). Posterior portion of the vestibule above the perineal
body. Dimple in fossa implies no prev. pregnancy
Urethra
Paraurethral glands
Hymen-single opening , cryptiform,linear,imperforated
Corniculae myritiformes : hymen tags after birth












- Extends from hymenal ring to the fornices around the cervix
- Non keratinised stratified sq. epithelium
- Blood is supplied by the vaginal artery from the internal iliac
artery
- No mucous glands or hair follicles
- Adenosis occurs if exposure (gestational) to DES
- Inner circular and outer longitudinal muscle coats
- 8 cm in length adult
- Immediate proximity of posterior fornix to the pouch of
Douglas
- The pH of the vagina is 4.5 and is due to Doderlein`s bacillus,
which breaks down glycogen to lactic acid


- Surrounded by 3 layers : - visceral peritoneum
- Myometrium
- Endometrium
- Normally anteverted and antiflexed
- Blood is supplied via the uterine artery from the internal iliac artery
- Cervix and uterine corpus , joined by the isthmus
- Isthmus is where the endocervical epithelium changed to the endometrial lining
- Endometrial lining varies from 2-10 mm thick
- Isthmus is lower uterine segment in pregnancy
- 2-3 cm length (cervix)
- At the external cervical os, the squamous epithelium changed to simple columnar (squamocolumner
junction)

- Four paired sets of ligaments are attached :
- Round ligaments : extending between the labium majus and the anterior aspect of the uterus (in
front of the Fallopian tube)
- Uterosacral ligaments : condensation of endopelvic fascia , which
insert into the posterior-inferior portion of the uterus at the level of the isthmus.
The round ligament in IN
FRONT of the broad ligament
- Cardinal ligaments : extending from the pelvic fascia on the lateral walls and inserting into the
lateral portion of the cervix and vagina.
- Pubocervical ligaments : passing around the anterior of the bladder to the posterior aspect of
the symphysis pubis.

* For support the UTEROSACRAL ligaments and CARDINAL ligaments are the most important in preventing
prolapsed.

- Four peritoneal folds :
1-Vesicouterine fold (anterior), from the isthmus to the bladder
2-Rectouterine fold (post), from the posterior wall of the uterus to the rectum
* The pouch of Douglas lies between the two folds
3-Broad ligaments (laterally, paired), from the side of the uterus to the lateral wall of the pelvis.
4-The mesosalpinx is the fold containing the fallopian tube



- 10 cm in length
- Enclosed in the medial 4/5ths of the superior aspect of the broad ligament
- Segments : - interstitial
- Isthmus
- Ampullary (most common site of ectopic pregnancy)
- Fimbriated portion
- Ciliated columnar epithelium
- Uterine and ovarian arteries supply blood


- 3 by 2 by 2 cm
- The only intrabdominal structure not covered by peritoneum
- Located on the superior surface of the broad ligament, suspended between the ovarian ligament
(medially) and the suspensory ligament (laterally and superiorly)
- Found in the ovarian fossa of Waldeyer), which is lateral to the pelvic walls , anterior to the ureter
and hypogasteric vessels and posterior to the external iliac vessels



- Blood supply : long ovarian arteries from the abdominal aorta , below the renal arteries
- Veins : right ovary drains to the inferior VC , the left ovary drains to the left renal vein

















- 25-30 cm from renal pelvis to the bladder
- Cross under the ovarian vessels , in front of the bifurcation of the
common iliac artery
- Located in the true pelvis, anterior to the hypogastric vessels , on
the side of the cervix and beneath the uterine artery (remember
: water under the bridge ).
- It run close to the internal vaginal fornix and passes to the
trigone of the bladder.

**Please refer to OB/GYN recall for more illustrations

Development and Congenital Abnormalities of the
Reproductive System

Prepared by: Ayah M Boudal & Nedaa bhkali
Source: Tarek Arab sheets


Embryological development of the ovary
Thickening of the peritoneal epithelium on the ventro-medial surface of urogenital ridge
occurs,thus a genital ridge is formed , parallel to mesonephric ridge.
5
th
week, sex cord formed
The primitive gonad is of multiple origin ( coelomic epithelium of the genital ridge , the
underlying mesoderm and primitive germ cells)
3 weeks gestation , primordial germ cells appear mixed with other cells in the endoderm
of the yolk sac wall of the primitive hindgut
At 8 weeks, it is contained in the undierenated urogenital ridge. Proliferaon results in
formation of oogonia that are incorporated into sex cords.
First evidence of follicles is seen at 20 weeks, granulose cells (coelomic epithelium) and
theca cells (mesenchymal origin) are evident . There are 200,000 follicles present at 20
wks and 300,000 present at 7 yrs of age.
Regression of primary sex chords results in formation of the rete ovarii.








The paramesonephric (Mullerian) ducts are the source of the:
Upper vagina
Uterus
Fallopian tubes

Absence of a Y chromosome results in regression of the mesonephric system and development of the
paramesonephric .

M ducts develop at 2-4 wks at the genital ridge, terminate caudally by opening into urogenital
sinus , and open cranially at a point to become tubium osteum
At 6 weeks gestaon . a groove forms in the coelomic epithelium of the paired urogenital ridges.
The two ducts fuse at the urogenital septum , forming the uterovaginal primordium . The distal
point of fusion in known as Muller`s tubercle .
Dissoluon of the septum between the 2 ducts leads to a single uterine fundus.
Degeneraon of mesonephric ducts from 10-16 weeks.
Derivatives:
Adjacent mesenchyme gives the : Myometrium & endometrium
Paramesonephric duct gives the : Glandular epithelium of fallopian tubes,uterus,cervix
At 12-20
th
weeks, vaginal plate formation takes place from the endoderm of the
urogenital sinus (controversial).


Prior to week 7 , same appearance of male and female genitalia
Elongation of the genital tubercle into a phallus takes place in males
In female , differentiation of the urogenital membrane (ectoderm and endoderm) into
genital folds laterally (give rise to labia majora) and urogenital folds medially (give rise to
labia minora and prepuce of clitoris ) occures.
By week 12, the female genitals are evident
The hymen is perforated at birth time
Abnormal development of the ovaries
Uncommon
Duplication or absence of ovarian tissue may occur
Turner`s syndrome (45 XO) is associated with lack of gonadal development , thus streaked
primitive ovaries in this condition.
Anomalies of paramesonephric ducts and urogenital sinus
Anomalies of fallopian tubes , uterus , cervix , and vagina are uncommon and are caused by
teratogenesis , genetic inheritance and multifactorial expression.

Agenesis (lack of development)
Hypoplasia ( incomplete development)
Atresia ( incomplete canalization)
Completely separate development
Variations of extent and level of fusion
Fallopian tubes :
Aplasia or atraemia of the distal ampullary segment occurs , most commonly unilateral.
Complete duplication is rare , but distal duplication and accessory ostia are common.
Cervix and uterine fundus :
In Mullerian agenesis , complete lack of development of paramesonephric system occurs. Usually ,
incomplete development of the fallopian tubes is associated with absence of uterus , cervix and most
of the vagina.
Mullerian agenesis occurs in women who are normal karyotypic and phenotypic females.













More commonly include :
Imperforate hymen
Longitudinal and transverse vaginal septum
Vaginal atresia
Double vagina
Absence
Imperforate : least severe abnormality
Occurs at the site of vaginal plate formation.
Blocks menses
Transverse vaginal septum similar but allows menses because of a sinus or tract
Usually discovered on examination after intercourse impeded.

Atresia: Upper vagina and cervix affected if cranially
placed , uterine fundus +tubes unaffected




Double vagina : Midline longitudinal septum is present thus deformity. Associated with double
cervix

Agenesis : Most extreme vaginal
abnormality
The uterus is usually absent






Partial unilateral development of para mesonephric ducts : absence of ipsilateral kidney
Uterus didelphys , one of 2 vaginas exisng as blind pouch : renal agenesis on the side of
pouch
Mullerian agenesis : pelvic kidney, horseshoe shaped kidney , duplication of collecting system

Sexual ID in case of ambiguous genitalia :

Female pseudohermaphroditism :
Due to masculinisation in-utero, the infant presents with ambiguous genitalia
Enlargement of clitoris is the most conspicuous abnormality
Internal genital development is normal
Male pseudohermaphroditism :
If 46 XY, tescular feminizaon syndrome can result in development of external genitalia
like those of a female (X linked recessive disorder).
The disorder is not recognized until failure of menarche at puberty
Testes are undescended
External genitalia normal on exam , but scanty pubic hair
True hermaphroditism :
Rare
Dual development of testes and ovaries
Usually 46 XX

The Menstrual Cycle
Prepared by: Badr Rajb (edited by Wafaa Al-Ahmadi)
Source: Obstetrics & Gynecology AT Glance + Tarek Arabs sheet

Definition
Menstrual refers to cyclic uterine bleeding experienced by most women of reproductive age.
Normal menstruation
Menarche before 16 years (average age at 12 years).
Menopause aer 40 years.
Menstruaon not more than 7 days (52 days).
Blood loss not more than 80 ml/day.
Cycle length 21-40 days (302).
No intermenstrual bleeding.
Hormonal changes of the menstrual cycle cause ovulation & induce changes that prepare tha
endometrium for implantation, should conception occur. Further changes are manifested in the cervix,
vagina, & breast.
For menstruation to occur, the hypothalamus-pituitary-ovarian axis must be intact.
Ovarian changes
Theres monthly increase in FSH which stimulates the growth of primordial follicles. One develops,
& ovulaon takes place on day 14 on the surge of LH.
Theres 3 phases of ovarian changes:
Follicular phase:
- Granulosa cells proliferate, with fluid filled spaces forming the antrum of the primary follicle.
Changes occur resulting in the formation of the vesicular follicle & finally the mature Graafian
follicle.
- The oocyte is enlarged, & surrounded by the zona pellucida & cumulus oophorus.
- Granulosa cell have FSH receptors that respond to FSH to produce E2.
- Theca cells (interna) are vascular & have LH receptors, producing androgens which stimulate
granulosa cells to secrete E2.
- High level of E2 cause ve feedback on LH & FSH.
- At mid-cyclic feedback is +ve on LH, thus a surge in LH concentration occurs, with subsequent
ovulation.
LH stimulate theca interna cells which secrete androgens ----- FSH + androgens stimulate granulosa cells
--------- producon of E2.



Ovulatory phase:
- The distended follicle ruptures, & the ovum is released into the peritoneal cavity the ovum is
surrounded by the zona pellucida & corona radiata.
- Swept into uterine tubes by fluid flow, caused by the beating cilia in fimbriae.
- The follicles enlarge, but if theres failure to ovulate, they degenerate into atretic follicles.

Luteal phase:
- Ruptured follicle fills with blood, forming corpus haemorrhagicum.
- Granulosa cells, theca cells, clotted blood replaced by lipid cells (luteal cells), thus the corpus
luteum is formed.
- Corpus luteum secretes E2 & progesterone.
- High E2 & progesterone impose ve feedback on LH & FSH.
- If pregnancy occurs, the corpus luteum changes to that of pregnancy, & no more cycles occur. If
pregnancy take place, the corpus luteum degenerates.
- An increase in FSH & LH take place in preparation for the next cycle.

Uterine changes
There are 3 phases:
Proliferative phase (pre-ovulatory):
- Takes place during follicular phase of ovarian cycle.
- High E2 causes rapid growth of the endometrium, epithelium, uterine glands. The glands are
NON-SECRETORY.
- Increased uterine blood flow.
- Increased contraction & excitability of the myometrium.

Secretory phase (post ovulation):
- Coincides with the luteal phase of ovarian cycle.
- Developed corpus luteum secretes predominantly progesterone, & estrogen in small amounts.
- Further changes in the endometrium, increased blood flow, edematous.
- Endometrial glands enlarge, coil, & become SECRETORY (glycogen, sugars, & amino acids).
- Deposition of the fats & glycogen in endometrial cells take place.
- Arteries prominent & coiled.

Menstrual phase:
- Occurs only if fertilization & implantation dont occur.
- If no implantation, no hCG is produced & therefore the corpus luteum regresses with a sharp
decrease in E2 & progesterone level.
- Reduction of endometrial tissue, & ischemia followed by necrotic foci giving subsequent spotty
hemorrhages which are manifest as menstrual blood flow.
- Menstruam (blood, tissue debris & ovum), accumulate in the uterine cavity, & is expelled by
uterine contractions.
- Blood containes brinolyc enzymes, & usually does not coagulate, thus it ows for 3-5 days.

Changes in the uterine cervix
a) Follicular phase increased E2: Mucus thin & alkaline.
b) Luteal phase increased progesterone: Mucous thick, tenacious, cellular.

Changes in vagina
a) Follicular phase increased E2: vaginal epithelium cornied.
b) Luteal phase increased progesterone: epithelial proliferation with leucocytes.

Cyclic changes in breast
a) Follicular phase increased E2: proliferaon of mammary ducts.
b) Luteal phase increased progesterone: growth of lobules & alveoli, swelling of breast &
tenderness.















Day 1 4: menstruation.
Day 5 13: proliferative phase.
Day 14 28: luteal/secretory phase.



Control of ovarian hormones:
Gonadotrophins (FSH. LH):
FSH from the anterior pituitary stimulate the growth of ovarian follicles.
FSH & LH are needed for final maturation of follicles.
LH surge at mid cycle causes ovulation & corpus luteum formation.
LH smulate secreon of E2 & progesterone from the corpus luteum.

Hypothalamic components:
Hypothalamus secrete GnRH in episodic bursts (60-120 mins) to smulate anterior pituitary to
secrete FSH & LH.
GnRH administration in continuous infusion results in down regulation of the receptors, & LH
secretion decreased to zero level.
GnRH administration episodically stimulates LH.
GnRH incresase GnRH decrease
Late follicular phase (due to +ve feedback of E2,
causes LH surge).
Secretory phase (because of progesterone)
At end of the cycle (due to ve feedback of E2 &
progesterone.
Negave feedback of E2 & progesterone

Feedback effects:
- Moderate levels of E2 inhibit both FSH & LH during early part of the cycle. Inhibin also inhibits
FSH.
- Rise of E2 36-48hrs before ovulaon causes +ve feedback on LH (LH surge). Ovulaon occurs 9 hrs
after LH peak.
- FSH peaks at mid cycle despite small rise in inhibin.
- During luteal phase LH & FSH are low because of elevated E2, progesterone & inhibin.

Control of the cycle:
- Prostaglandins causes regression of corpus luteum 3-4 days before menses.
- E2 & progesterone start to decrease, FSH & LH start to increase.
- New follicles develop under the effect of FSH & LH to ovulation & formation of corpus luteum.
- Rise E2, progesterone & inhibin with decrease both FSH & LH before luteolysis.

Clinical points:
Hormonal assays:
- To determine if ovulation occurred:
- Serum progesterone > 10 nmol/l indicate ovulaon has occurred.
- Blood should be drawn in the mid-luteal phase (day 21).
- The results can only be interpreted if a menstrual period occurs 7 days aer sampling.





PMS:
- These are clinical psychological, behavioral & physical symptoms starting at the luteal phase &
ending during menstruation.
- 95% women suer from it.
- Unknown etiology.

Clinical features:
- Tension.
- Breast pain.
- GIT upset.
- Depression.
- Loss of control
- Irritability.
- Aggression.
- Insomnia.
Pelvic Mass
Prepared by: Wafaa Al-Ahmadi
Source: On call obstetrics & gynecology + Toronto Notes 2008 + Approach to the Patient with a Pelvic
Mass (ptt) done by Lloyd D. Holm, D.O. (Associate Professor Department of Obstetrics and Gynecology
university o Nebraska medical center) + BPL management of pelvic mass - Done by group B 2008



The adnexa comprise the fallopian tubes, ovaries, & round ligaments.
Pelvic mass commonly arise from the adnexa & refered as adnexal mass.
Pelvic mass also can arise from the uterus as well as from organs other than reproductive
organs such as bladder & GI tract.
Differential diagnosis of an adnexal mass is vast & depend on the patients age.
Adnexal masses are uncommon in the premenarchal & post-menopausal patients, &
when they are encountered, malignancy should be suspected.
In contrast adnexal masses are commonly found in women in the reproductive age range
because the frequency of functional or physiological cysts (this cysts result from the
process of ovulation & usually resolve spontaneously.


Pressure/fullness
Pelvic pain
Abdominal pain
Abdominal distention
Dyspareunia
Vaginal bleeding
Urinary frequency


GI symptoms
Nausea.
Dyspepsia.
Obstipation (sever or complete constipation).
Painful bowel movement.



Differential diagnosis of pelvic mass
Gynecological:
Ovarian:
Functional cysts (always benign):

Corpus luteum cyst:
It could be discovered incidentally by obstetric
examination or annual examination.

Are approximately 4 cm in diameter & result from hemorrhage in the corpus luteum 2 or 3
days after ovulation? Because these cysts may rupture & result in intra-abdominal bleeding,
they can mimic tubal pregnancies. Rupture usually occurs late in the menstrual cycle & is
associated with acute abdominal pain, which usually lasts less than 24 hrs but may be present
for up to 1 week.

Follicular cyst:
The most common cystic masses found in the ovary. They result from either failure of the
mature follicle to ovulate or failure to an immature follicle to resorb or undergo atrasia. Most
follicular cysts are asymptomatic & range in size from several millimeters to 8 cm cysts.
Theca lutein cyst:
Developed from overstimulation of the ovaries by hCG. They are encountered in patients with
molar pregnancies & in those who undergone ovulation induction for infertility.
Hemorrhagic cyst

Polycystic ovary

Endometrioma:
It could develop in patients with endometriosis involving the ovaries.
These cysts are filled with old blood that has the appearance of chocolate,
& therefore, endometriomas are also called chocolate cysts.
Tube-ovarian abscess
Luteoma of pregnancy
Benign neoplasms:
Dermoid cyst most common
Malignant neoplasns:
Epithelial cell most common > 40 years
Germ cell most common < 20 years
Metastasis (e.g. Krukenberg tumor from gastric cancer)

Tubal:
Ectopic pregnancy.
Paratubal cysts:
Paratubale cyst are found adjacent to the fallopian tubes. They are predominantly
cystic & are asymptomatic unless they undergo torsion. Paratubal cysts found at the
fimbriated ends of the tube are also referred to as hydatid cysts of Morgagni.
Pyosalpinx/hydrosalpinx.
Primary fallopian tube neoplasms.
Uterine:
Intrauterine pregnancy
Adenomyosis of the uterus
Fibroid
Endometrial cancer
Leiomyosarcoma
leiomyomata
Imperforated hymen
Hematometra/pyometra
Congenital anomaly of the uterus:
Bicornuate uterus.
Rudimentary uterine horn.
Didelphic uterus.

Non-gynecological causes:
Gastrointestinal:
Appendiceal abscess
Diverticular abscess
Diverticulosis, diverticulitis
Carcinoma of the rectum/colon

Genitourinary:
Distended bladder (urinary retention).
Pelvic kidney.
Carcinoma of bladder.

Miscellaneous mass:
Abdominal wall abscess, seroma, or hematoma.
Retroperitoneal neoplasm.




Evaluation of pelvic mass
History:
Important historical points:
If the patient is pre-menarchal or post-menopausal?
Adnexal masses are most likely to be malignant in those patients, compared with
women in the reproductive age group.
Last menstrual period
Women who have missed menstrual period should have intrauterine & ectopic
pregnancy ruled out
Relation of the mass with menses
History of the mass;
o Duration (chronic pelvic mass include leiomyomata, hydrosalpinges, &
endometriomas).
o How it had been discovered
o Any changing in the mass ( increase, decrease or the same size).
o Does the patient have a Hx of weight loss & vague abdominal symptoms such as
anorexia, dyspepsia, distention, nausea, & dull pain or discomfort these
symptoms can be caused by ovarian malignancy.
o Other associated symptoms change in bowel habits, any gastrointestinal
bleeding, haematuria, dysuria, change in urine color.

Examination:
General:
Wt loss
Anemia
Jaundice
Lymphadenopathy
Breasts
Auscultation of heart + lungs
Effusion.

Abdomen:
Masses (all characteristics of the mass).
Distention from the mass or hemorrhage.
Ascites may be associated with ovarian malignancy.

Pelvic:
Masses (also with all characteristic of mass).
External genitalia & vagina: vaginal bleeding in ectopic pregnancy, intrauterine
pregnancy, uterine fibroids, or sarcoma.
Cervix: cervical motion tenderness may be present with PID or tubo-ovarian adcsess.
Uterus: enlargement with or without tenderness in leiomyomata, sarcoma, or
intrauterine pregnancy.
Adenxa: mass may be palpable, either unilateral or bilateral, with or without
tenderness. Fixed & nonmobile adenxa is suggestive of endometrioma, PID, or ovarian
malignancy.
PR.

Important signs you have to look for
In Ectopic pregnancy, ovarian torsion, cyst rupture, bleeding hemorrhagic cyst or pelvic abscess:
toxic looking,
fever
severe lower abdominal tenderness
muscle rigidity
peritonitis

Abscess ruptures :
abdominal distension
shock and tachycardia
PCOS :
obesity (centripetal)
hirsutism
acne

Investigations

CBC with differential:
A CBC with differential should be obtained to help with the diagnosis of masses associated
with PID, such as pyosalpinx or tubo-ovarian abscess.
It can also detect anemia in those patient with intra-peritoneal bleeding from any source.
Rapid urinary pregnancy test:
A pregnancy test should be obtained in all patient of reproductive age to rule out either
intrauterine or ectopic pregnancy.

Serum cancer antigen:
Cancer angen 125 (CA-125) is a tumor marker for ovarian epithelial cancers.
Unfortunately, CA-125 is non-specific & is also elevated in adenocarcinoma of the uterus
& colon, endometriosis, PID, IBD, pregnancy, & hepatitis.

Serum human chorionic gonadotropin (hCG) & alpha-fetoprotein (AFP):
Serum hCG & AFP are tumor markers in germ cell tumors of the ovaries. These tumors
make up nearly 20% of all ovarian neoplasms, & most occur in young women.

Ultrasound examination:
U/S examination will confirm the presence of a pelvic mass & furthermore will provide
information concerning the size, bilaterality, origin, & consistency of the mass, whether
cystic solid, or complex.
Ultrasonography is a method of choice in the radiological evaluation of an ovarian mass.

Computed tomography (CT):
CT scan can sometimes supplement the information obtained by U/S examination. CT
scan of the pelvis should be performed with contrast to opacify & therefore delineate the
bowel.
A CT scan in especially helpful in the evaluation of masses in the pelvic side wall.
A CT scan is also helpful in staging pelvic malignancies, detecting peritoneal implants, &
delineating pelvic abscess during drainage procedure.

Magnetic resonance imaging (MRI):
MRI provides soft-tissue contrast resolution that is superior to that obtained by U/S
examination or CT scan. It specially helpful in the assessment of conditions that result in
uterine enlargement such as congenital anomalies of the uterus, leiomyomata, &
adenomyosis, MRI can provide information on the size, number, & location of
leiomyomata.








Management

Ectopic pregnancy:
Goal of treatment: be conservative.
Surgical: (laparoscopy)
Linear salpingostomy if tube salvageable.
Salpingectomy if tube damaged or ectopic is ipsilateral recurrence.
May require lapratomy
Medical:
Methotrexate 50 mg/m
2
body surface area; given in a single IM dose
Follow beta-hCG levels weekly until beta-hCG is non-detectable.
Fallopian tube neoplasms:
Staging and treatment is similar to ovarian cancer.

Tubo-ovarian abscess:

Hospitalization
Adequate hydration
Analgesics
I.V antibiotic ( clindamycin, aminoglycoside )
Ultrasound guided aspiration

Endometrioma:
OCP, progestin, symptomatic relief of pain, gonadotropin releasing hormone agonist (6
month unless combined with add back estrogen +/- progestin
Endometrioms larger than 2 cm are best treated surgically
PCOS:

Weight reduction
OCP
Spironolactone for hirsutism
Progestin
Insuline sensitizing agent
Clomiphene citrate (for women who wanna get pregnant)
Surgical Rx ovarian drilling with laser or diathermy, laser hair removal

Ovarian Cancer Management
Guidelines for staging come from the International Federation of Gynecology and
Obstetrics (FIGO). Stages include:
Stage I (Growth limited to the ovaries, and subdivided into Stage IA, IB, and IC,
depending on the number of ovaries involved, presence or absence of ascites,
tumor cells on the external surface of the ovaries or in peritoneal washings)
Stage II (Growth beyond the ovaries, but limited to the pelvis. Stage II is further
subdivided into IIA, IIB, and IIC, depending on the specific areas of extension,
presence of ascites, and tumor cells in peritoneal washings)
Stage III (Growth out of the pelvis, but still within the epithelial surfaces of the
abdominal cavity. This is subdivided into IIIA, IIIB, and IIIC, depending on the
location of the growth and its size.)
Stage IV (Distant metastases outside the confines of the abdominal cavity or
within the liver parenchyma).
Surgical treatment options include local excision, TAH/BSO, and such debulking
procedures as omentectomy and bowel resection.
Early ovarian cancer might optimally be treated with TAH/BSO, but instead, a simple
oophorectomy is performed to preserve the woman's childbearing capacity.

Leiomyomas
Most pt dont require treatment
Medical:
GnRH-a up to 6 months, shrink broid and improve symotoms
Surgical:
Hystrectomy: most common indication
Liomyomectomy: preserve fertility
Uterine artery embolization: reduce menstrual flow
Adenomyosis:
No effective medical treatment
Hysterectomy is curative.




Pelvic Pain
Prepared by: Wafaa Al-Ahmadi
Sources: Obstetrics & Gynecology Recall + Obstetrics & Gynecology On Call + Obstetrics & Gynecology
At Glance + Tareq Arabs sheet


It could be either acute or chronic pelvic pain
Acute pelvic pain:
Acute pelvic pain requires aggressive management because of the possibilities that a life-
threatening condition exists.
Gynecological causes:
Ectopic pregnancy:
o In all reproductive-age women, the first priority in evaluating acute pelvic pain is to
rule out the possibility of ruptured ectopic pregnancy.
o Tubal rupture can lead to hemoperitoneum & shock.

Acute pelvic inflammatory disease (PID):
Is an ascending bacterial infection that usually present with high fever, acute pelvic pain, &
evidence of cervical emotion tenderness in sexually active women.
Rupture of ovarian cyst:
Intra-abdominal rupture of a follicular cyst, corpus luteum, or endometrioma, is the
common cause of acute pelvic pain the may be so acute & sever as to cause syncope. The
condition is usually self limiting with limited intra-peritoneal bleeding.
Adnexal torsion:

Is seen most commonly in adolescent or reproductive-age women. By twisting on its
vascular pedicle, any adnexal mass (ovarian dermoid, hydatid of Moegagni) can cause
acute, sever pain by suddenly compromising its blood supply. The pain will frequently wax
& wane with associated nausea & vomiting.


Threatened, inevitable, or incomplete abortions are generally accompanied by midline
pelvic pain, usually of crampy, intermittent nature.
Degeneration of fibroid or ovarian tumors: May cause, localized, acute, sharp, or aching
pain.
Hemorrhage into the cyst/neoplasm.
Torsion of pedunculated fibroid.
Endometritis.
Labour.
Placenta abruption.
Non-gynecological:
Gastrointestinal causes:
Appendicitis: is the most common acute surgical condition of the abdomen, occurring in all
age groups. Classically, the pain is initially diffused & centered in the umbilical area but
after several hours, localizes to the right lower quadrant (McBurreys point). It is often
accompanied by low grade fever, anorexia, & leukocytosis.
Diverticulitis: occurs most commonly in older women. It is characterized by left-sided
pelvic pain, bloody diarrhea, fever, & leukocytosis.
Mesenteric lymphadenitis: most often follows an upper respiratory infection in young
girls. The pain is usually more diffuse & less sever than in appendicitis.
IBD
Genitourinary causes:
UTI: cystitis, pyelonephritis, renal calculi) can cause acute or referred suprapubic pain,
pressure, and/or dysuria.
Chronic pelvic pain:

It is refer to unrelieved pain that has continued to be a major, disabling condition for at least 6
months.
Gynecological causes:
Dysmenorrhea: is the most common cause of chronic pelvic pain. It is defined as a cyclic
uterine pain occurring before or during menses. The pain is located in the lower abdomen & is
frequently described as a painful, crampy sensation that often accompanied by nausea,
vomiting, headache, swelling, sweating, fatigue, & lightheadedness.
Primary dysmenorrhea: is not associated with pelvic pathology, and is thought to be due
to excessive prostaglandin production by the uterus.
Secondary dysmenorrhea: usually it is due to acquired conditions (e.g. endometriosis).


Endometriosis: the presence & growth of endometrial glands & stroma in locations outside
the endometrial cavity of the uterus. Endometriosis most often involves the ovaries, the cul-
desac, the uterosacral ligaments, the rectosigmoid, & the posterior cervix. The classical
symptoms of endometriosis include dysmenorrhea, dyspareunia, dyschezia, & infertility. The
pain range from dysmenorrhea to sever, intractable, continuous pain which may be disabling.
The severity of the pain need not correlate with the degree of pelvic pathology.

Adenomyosis: the presence & growth of endometrial glands & stroma in the uterine
myometrium at a depth of 2.5 mm from the basal layer of the endometrium. It is a common
condion (usually found in women 35 to 50 years old) & most women are asymptomac, but
some patient may have dysmenorrhea & menorrhagia. An enlarged, boggy uterus, that is
mildly tender on palpation is characteristic.

Fibroids: are the most common (benign) tumor found in the females pelvis. They may cause
pain either by putting pressure on the adjacent organs or by undergoing degeneration.



Retained ovarian syndrome: is characterized by recurrent adnexal pain after hysterectomy.

Genital prolapse: may lead to complaint of heaviness, pressure, a dropping sensation, or
pelvic aching.

Chronic PID: characterized by continued pelvic pain, usually as a result of hydrosalpinx,
tubo-ovarian cyst, or pelvic adhesions.

Pelvic congestion syndrome: syndrome caused by pelvic varicosities that result in pelvic pain
or heaviness that is worse during the premenstrual period, after prolonged standing, & after
intercourse.

Non-gynecological causes:
Gastrointestinal:
IBS.
IBD.
GI neoplasm.
Constipation.
Partial bowel obstruction.
Diverticulitis.

Genitourinary:
Urinary retention.
Urethral syndrome.
Interstitial cystitis.

Others:
Referred pain (as in disk herniation).
Hernia formation.
Sexual/physical/psychological abuse.
Depression/anxiety/somatization.



Important points in the history:
Pain analysis (character, radiation, quality, intensity, & location of the pain)?
Temporal aspect (typical pattern, throughout the day/week/month, cyclicity, duration).
Her LMP: if the pt missed her menstrual period, either intra-uterine or ectopic pregnancy
should be suspected.
Relation of the pain to menstrual cycle & menorrhagia, abnormal bleeding (pain is correlate
with menses is suggestive of endometriosis, adenomyosis, primary dysmenorrheal).
Is the pain exacerbated by bowel movements, urination, sexual intercourse, physical activity
suggestive of endometriosis.
Is the pain associated with abnormal vaginal bleeding? suggestive of leiomyomata or
adenomyosis, if the patient is pregnant, tubal pregnancy or spontaneous abortion should be
ruled out.
Previous episodes.
Degree at which the pain disrupts daily activity.
Events that happened concurrent with pain onset (IUD, Rape, lifting heavy objects).
Pain medications.
Symptoms of stress/depression.
Recent changes in the bowel habits/urinary changes.
Recent onset of symptoms of GIT/GUT problems.
Gynecological Hx:
o Infertility Hx of infertility is consistent with endometriosis or pelvic adhesions from
prior PID.
o PID pelvic adhesions or hydrosalpnix.
o Past gonococcal/chlamydial infection.
o Endometriosis.
o Time of the last pelvic exam.
o Past abortions.
o OCP use.
o Sexual Hx (dyspareunia, frequency, effect of pain).
Past Hx:
o All past surgical procedures.
o Musculoskeletal disease.
o History of past sexual abuse, physical, emotional.

Physical examination:
Pelvic exam with attempt to reproduce & localize pain:
Endometriosis will yield a fixed retroverted uterus with tenderness uterosacral nodularity.
Chronic salpingitis may be suggested by bilateral, tender, irregular enlarged adnexae.
Prolapsed may present with pain/back pressure.
Abdominal wall examined for evidence of myofascial trigger points:
o Iliogypogastric T12, L1.
o Ilioinguinal T12, L1.
o Genitofemoral L1, L2.
Palpate for tenderness.
Patient straight leg raises or partial sit-up.
Pts still tender injected with marcain, & chronic abdominal wall pain confirmed if pain decrease
50% & outlasts duraon of marcaine.
Investigations:
CBC with differential: will help to diagnose infection. Sever anemia is suggestive of bleeding from
a ruptured tubal pregnancy or from hemorrhagic ovarian cyst.
ESR.
Beta hCG.
Urinanalysis.
Occult blood.
Liver function test.
Pelvic U/S will detect pelvic masses such as uterine leiomyomata & adnexal masses as well as
abdominal masses. Ultrasonography will not detect pelvic adhesions or pelvic endometriosis.
Diagnostic laparoscopy as last resort.
IF INDICATED GIT X-ray, endoscopy, cystoscopy, IVP, Lumbosacral X-ray, CT scan, MRI,
orthopedic consultation.
Treatment:
Conservative.
Medical treatment:
o OCP/GnRH agonists may relive pain in those with mid-cyclic, premenstrual, menstruation
exacerbated pain, ovarian pathology (peri-ovarian adhesions/recurrence functional
cysts).`
o NSAIDs.
o TCAs
The following are potential options:
o Unilateral adnexectomy for unilateral pain.
o TAH.
o Pre-sacral neurectomy.
o Uterosacral nerve ablation.
o Uterine suspension.
o Lysis of adhesions.
Full psychosomatic evaluation prior to surgery.
Anesthesia:
85% of patients have abdominal wall trigger points that respond to biweekly injections local
anesthetic.
AMENORRHEA
Prepared by: Jameel Khalid Rasheedi (Dr.JKR)
Sources: Toronto Notes 2008 + Kaplan USMLE 2008 + Ob/Gyn at Glance + Gynecology Illustrated +
Essentials of Ob/Gyn (Hacker) + National Medical Series + First Aid for Ob/Gyn



Amenorrhea is the absence or cessaon of menstruaon for 6 months or longer and can be Primary or
Secondary
PRIMARY: is the absence of menses at age 14 years without development of secondary
sexual characteristics or at age 16 years regardless of secondary sexual characteristic
development. ((menses have never occurred))

SECONDARY: is the cessaon of menses for 6 months or a three-cycle interval in women
who have been menstruating regularly.



According to . . .

Site of lesion Hormonal state
HYPOTHALAMIC : FSH/LH levels
1-Congenital lack of GnRH e.g. Kallmans syndrome.
2-Pituitary stalk compression: Tumors, granulomas,
irradiation, infiltrative disorder.
3-Decrease GnRH release: Stress, anorexia,
hyperprolactinemia, severe weight loss, extreme
exercise due to catecholamine & endorphin.

PITUITARY : FSH/LH levels
1-Hypopituitarism duo to Sheehans syndrome
(Simmond disease) : Pituitary infarction from
hypotension during postpartum hemorrhage.
2-Primary Hypopituitarism.
3-Tumors: adenoma, Craniopharyngioma, prolactin-
secreting tumors.
4-Hemosiderosis: Iron deposition in pituitary that
impairs its function.

OVARIAN : FSH/LH levels
1-Menopause.
2-Premature ovarian failure.
3-Savages syndrome: Ovarian resistance to FSH/LH
4-Enzyme defects: commonly 17-hydroxylase.
5-Gonadal dysgenesis : Turners syndrome 45X
6-Chronic anovulation: Polycystic ovary syndrome
PCOS, ovarian/adrenal tumor.
7-Radiation, chemotherapy.



HYPERGONADOTROOIC :
1-Turners syndrome 45X.
2-Premature ovarian failure.
3-Gonadal dysgenesis: XYgenotype, Swyer syndrome
4-Gonadal agenesis.
5-Resistant ovary syndrome (Savages syndrome).
6-Galactosemia: an autosomal recessive deficiency
in galactose-1-phosphate uridyltransferase (toxic
effect of galactose metabolites led to oogonia.
7-Enzyme deficiencies: a- 17-hydroxylase (prevent
synthesis of sex steroid) have ovaries but not
functioning, present with absent 2ndry sexual cha. ,
HTN, hypokalemia and progesterone level.
b- aromataze enzyme.

HYPOGONADOTROPIC :
1-Anorexia (amenorrhea, bradycardia, dry skin,
hypothermia, lanugo hair).
2-Exercise.
3-Stress increased corticotropin-releasing
hormone decreased GnRH pulsatile secretion and
thus decreased secretion of FSH and LH.
3-Congenital lack of GnRH e.g. Kallmans syndrome.
4-Postpill: amenorrhea may occure 6 or more
months after patient stop taking OCP.
5-Medication: Birth control pills, phenothiazine
derivatives, reserpine.
6-Pituitary diseases: sella turcica, Pituitary tumors
Craniopharyngioma, Adenomas.

UTERINE : normal FSH/LH
1-Congenital mullerian (uterine/vaginal) agenesis
(Mayer-RokitanskyKuster-Hause syndrome)
2-Imperforate hymen
3-Transverse vaginal septum
4-Cervical stenosis
5-Intrauterine adhesions :Asherman's syndrome
6-Congenital absence of uterus.
7-Androgen insensitivity syndrome (Testicular
Feminization)(XY)

ENDOCRINE :
1-Hyperprolactinemia.
2-Hyper/hypothyroidism.
3-Hyperandrogenism : PCOS, ovarian/adrenal
tumor, testosterone injections.
4-Cushing's disease.



EUGONADOTROPIC :
1-Disorders of androgen excess: polycystic ovary
syndrome.
2-Disorders of the outflow tract or uterus:
-Mullerian agenesis (Mayer-RokitanskyKuster-
Hause syndrome)
-Androgen insensitivity syndrome (Testicular
Feminization)(XY)
-Intrauterine adhesions :Asherman syndrome
-Infection: Tuberculosis and schistosomiasis
may cause intrauterine scarring and adhesions.
Physiologic causes: Pregnancy, Lactation, Menopause, Prepubertal.
















Primary Amenorrhea


Is the absence of menses at age 14 years without development of secondary sexual characteriscs
or at age 16 years regardless of secondary sexual characteristic development. ((menses has never
occurred)) .
Prevalence: 1-2% of girls.


The two main categories of etiology, ANATOMICAL: Imperforate hymen, vaginal septum/agenesis, or
mullerian agenesis. HORMONAL: Androgen insensitivity syndrome, Gonadal dysgenesis(Turner Syndrome),
or hypothalamic-pituitary insufficiency.



Clinical Approach Based on Findings Regarding Breasts and Uterus.
By physical examination determine wither breasts are present or
not and by an ultrasound for uterus


A- Breasts present, uterus present: Differential diagnosis includes an imperforate hymen, a
vaginal septum, vaginal agenesis, anorexia nervosa, excessive exercise.
If non is the cause, then the workup should proceed as if for secondary amenorrhea.
* Imperforate Hymen & Transverse Vaginal Septum: three degrees are recognized








-Clinical features: Primary amenorrhea, pelvic pain of increasing severity, urinary
retention in longstanding case due to pressure of distended vagina.
- Examination: Palpable pelvic mass, bulging vaginal hymen but no lower vaginal bulging
in Transverse Vaginal Septum , MRI here is the diagnostic method of choice.
- Pregnancy must be excluded.
- Treatment: Surgical.

B- Breasts present, uterus absent : Differential diagnosis is Mullerian agenesis (Rokitansky-
Kuster-Hauser syndrome) and complete androgen insensitivity (testicular feminization).
* Testosterone levels and karyotype help make the diagnosis.

Mullerian agenesis : " Mayer-Rukitamisky-Kuster-Houser-Syndrom "
- Genetically normal females (46,xx).
- Absence of the Mullerian duct derivatives: fallopian tubes,
uterus, cervix, and upper vagina.
- Breasts are an endogenous assay of
ESTROGEN.
- Pubic & axillary hair are an endogenous
assay of ANDROGEN.
- When diagnose amenorrhea, always role
out PREGNANCY first.

_____________
*Gynecology illustrated

- Mullerian ducts do not give rise
to the ovaries.
- Mullerian Agenesis Triad:
1. Primary amenorrhea
2. (+) breasts but (-) uterus
3. (+) pubic and axillary hair

- Patients develop secondary sexual characteristics because ovarian function is intact.
- Normal pubic and axillary hair is present.
- Testosterone levels are normal female.
- One third of cases associated with congenital renal abnormality, ( intravenous pyelogram, US )
- 12% have skeletal lesion.
- Management: surgical neovagina.(Frank method : dilation of
vaginal pouch, or McIndoe vaginoplasty: using skin graft ), no hormones.

Androgen insensitivity :
- Genetically male (46,xy), with complete lack of androgen receptor function No respond to the
high levels of androgens internal Wolffian duct structures atrophy.
- With testicular Mullerian inhibitory factor present, the Mullerian duct derivatives involute.
- Without body recognition of dihydrotestosterone, external genitalia differentiate in a female
direction.
- Patients function psychologically and physically as females and are brought up as girls.
- Female secondary sexual characteristics (breast) are present because the testes do secrete
estrogens without competition from androgens & peripheral conversion of androgen.
- No (or scanty) pubic or axillary hair is noted due to Androgen insensitivity.
- Testosterone levels are normal male.
- At puberty, when primary amenorrhea is noted, the diagnosis is made.
- Management: 1- Testes removed at the age of 20 because the higher
temperatures associated with the intraabdominal position of the testes
lead to testicular cancer.
2- Estrogen replacement.
3- surgical neovagina.


C- Breasts absent, uterus present: Differential diagnosis is gonadal dysgenesis (Turner
syndrome) and hypothalamic-pituitary failure.
* FSH level and karyotype help make the diagnosis.

Gonadal failure (Hypergonadotropic Hypogonadism):
- Turner syndrome (45,x) is caused by the lack of one X chromosome, which is essential for
presence of normal ovarian follicles.
- Incidence 1/2500
- These patients develop streak gonads.
- Short status, webbed neck, cubitus vulgas, infantile genitalia, coarctation of aorta.
- No estrogen duo to absence of ovarian follicles.
- FSH levels are elevated because of lack of estrogen feedback to the hypothalamus and pituitary.
- No secondary sexual characteristics are noted.
- Other karyotype include: 46XX(pure gonadal dysgenesis), mosaicism, 47XXX, 46XY gonadal
dysgenesis (Swyer syndrome), Congenital adrenal hyperplasia (17-hydroxylase).
- Management: Estrogen and progesterone replacement for development of the secondary sexual
characteristics and prevent osteoporosis.



- Third commonest cause of
primary amenorrhea.
*Why testes removed at age of
20 ys not before?
- Cancer is rare to occure
before that.
- To allow full breast & puberty
development and linear
growth.

Second most common cause of
primary amenorrhea
Turner syndrome is the Single most common
cause of primary amenorrhea, accounting for
>50% of gonadal failure paents.
Hypothalamic-pituitary failure (Hypogonadotropic Hypogonadism):
- No secondary sexual characteristic but uterus present by ultrasound.
- FSH levels will be low.
A - HYPOTHALAMUS: stress, anxiety, anorexia nervosa, excessive exercise, tumors, TB,
sarcoidosis, congenital (KALLMAN's SYNDROME) :
- Insufficient GnRH production and also anosmia & color blindness.
- X- linked, male > female.
- The defect is in the area of the brain that produces GnRH, but it's also close to
the olfactory center.
- CNS imaging will rule out a brain tumor, MRI hypodevelopment of
olfactory sulci.
B- PITUITARY: Congenital ( empty sella turcica , atrophy ), adenoma, tumors ( prolactin
secreting & non-prolactin secreting ), exposure to chemical.
- Management: Estrogen and progesterone replacement for development of the secondary
sexual characteristics and prevent osteoporosis.








Breasts present, uterus absent Mullerian Agenesis (46,xx) Androgen Insensitivity (46.xY)
Cause of Uterus absent? Idiopathic MIF
Estrogen source Ovaries Testes
Pubic hair Present Absent
Testosterone level Female Male



Breasts absent, uterus present Gonadal Dysgenesis (4S.x) HPAxis Failure (46,xx)
FSH
Why No estrogen
No ovarian follicles
Follicles not stimulated
Ovaries?
"Streak"
Normal
Diagnostic test - CNS imaging















Breast Uterus
( - ) ( + ) 1
st
common(Gonadal failure, Hypothalamic-pituitary failure)
( + ) ( + ) Rare (same workup as 2
nd
amenorrhea)
( + ) ( - ) Common(Mullerian agenesis, androgen insensitivity)
( - ) ( - ) Very Rare , almost always 46,XY
Secondary Amenorrhea


Is the cessaon of menses for 6 months or a three-cycle interval in women who have been
menstruating regularly.
Prevalence: 4-5% of women (excluding pregnancy)


Can be classified by alterations in FSH and LH levels into:
-Hypogonadotropic (hypothalamic or pituitary dysfunction)
-Hypergonadotropic (ovarian follicular failure)
-Eugonadotropic (pregnancy, anovulation, uterine or outflow tract pathology)

Anovulation:
- No corpus luteum is present to produce progesterone No progesterone-withdrawal bleeding.
- Anovulation is associated with unopposed estrogen stimulation of the endometrium.

-Polycystic ovary syndrome -Hypothyroidism TRH stimulate prolactin production.
-Medications (e.g., antipsychotics, antidepressants).
- Hypothalamic dysfunction:
-Tumor -TB -Sarcoidosis -Drugs: OCP(post pill amenorrhea)
-Stress -Exercise -Anxiety -Anorexia nervosa
- Pituitary:
- Adenoma -Craniopharyngioma -Prolactin-secreting tumors.
- Sheehans syndrome - Iatrogenic hyperprolactinaemia
- Ovaries:
-Premature ovarian failure: Loss of all ovarian follicles with cessation of menstruation
prior to age 40.
- elevated FSH
-Causes: intrinsic ovarian defect, genetic mosaicism, autoimmune(MG),
chemotherapy, radiation, infection(mumps).
- Savage syndrome (resistant ovary syndrome): a condition in which although follicles
are seen in the ovary by sonogram, they do not respond to gonadotropins.

Estrogen Deficiency: priming the endometrium will be atrophic with no proliferative changes taking place.
Causes of hypoestrogenic states: -absence of functional ovarian follicles.
-hypothalamic-pituitary insufficiency.

Outflow Tract Obstruction: - Asherman's syndrome: intrauterine synechiae(adhesion) that interfere with
normal endometrial growth and shedding.
Causes: - Extensive uterine curettage.
- Infection-produced adhesions.(TB)




1- Pregnancy Test: The first step in management of secondary amenorrhea is B-hCG test to rule out
pregnancy. If negative . . .

2-Thyrotropin (TSH) Level: hypothyroidism should be ruled out. If positive treatment is thyroid
replacement. If negative . . .

3- Prolactin Level:
-Medications. An elevated prolactin level secondary to antipsychotic or antidepressants, which
have an anti-dopamine side effect (hypothalamic prolactin-inhibiting factor is dopamine).
- Pregnancy is the most common cause of
secondary amenorrhea.
- When diagnose amenorrhea, always role out
PREGNANCY first.
-Tumor. A pituitary tumor should be ruled out with a CT scan or MRI of the brain.
-Tumor is < 1 cm treated medically with bromocriptine (Parlodel), a dopamine agonist.
-Tumor is > 1 cm usually treated surgically.
-Idiopathic. treatment is also medical with bromocriptine.
*Quinagolide: is a dopamine agonist tolerated better than bromocriptine, given daily.
*Cabergoline: is a dopamine agonist with long half life, given weekly.
*Radiotherapy: reserved to patients fail with medical and surgical therapy.
If the B- hCG is negative, and the TSH and prolactin levels are normal . . .

4- Progesterone Challenge Test (PCT) "provera test" : administer either a single 1M dose of progesterone
or 7 days of oral medroxyprogesterone acetate (MPA).

Positive PCT: - Any degree of withdrawal bleeding is diagnostic of anovulation.
- Cyclic MPA is required to prevent endometrial hyperplasia.
- Clomiphene ovulation induction if pregnancy is desired.

Negative PCT: - Absence of withdrawal bleeding is caused by
- inadequate estrogen priming of the endometrium .
- outflow tract obstruction.
If the PCT is negative . . .

5- Estrogen-Progesterone Challenge Test (EPCT): administer 21 days of oral estrogen followed by 7 days
of MPA.

Positive EPCT: - Any degree of withdrawal bleeding is diagnostic of inadequate estrogen.
- An FSH level will help identify the etiology.

An elevated FSH: suggests ovarian failure or Savage
A low FSH : - suggests hypothalamic-pituitary insufficiency.
- Order a CNS imaging study to rule out a brain tumor.
- CNS lesion empty sell syndrome, Sheehan syndrome.
- No CNS lesion Hypothalamic dysfunction

-Treatment: - estrogen-replacement therapy to prevent osteoporosis and estrogen-deficiency
morbidity.
- Cyclic progestins are also required to prevent endometrial hyperplasia.

Negative EPCT: - Absence of withdrawal bleeding is diagnostic of an outflow tract obstruction or
endometrial scarring (e.g., Asherman syndrome).
- A hysterosalpingogram (HSG) to identify where the lesion is.

- Asherman syndrome is treated by : - Hysteroscopic adhesion lysis.
- Estrogen stimulation of the endometrium.
- An inflatable stent is then placed into the uterine cavity to
prevent re-adhesion of the uterine walls.










_____________
*OB/GYN At a Glance

Infertility

Prepared by : Faisal Al-Gaows
Sources: Toronto notes2008 + Ob/gyn at glance




Fertility: the capacity to conceive and produce offspring.
Fecundity: the probability to conceiving during a single monthly cycle.
The fecundity of normal couple is 20% - 25% with cumulave 85% 90% chance of
pregnancy in 12 months
Infertility: Failure to conceive after one year of regular unprotected intercourse.
Primary infertility: no prior pregnancies
Secondary infertility: previous conception.




10-15% of couples
normally 75% of couples achieve pregnancy within 6 months, 85% within 1 year, 90% within
2 years
must investigate both members of couple


- Fecundity in women peak s at 25 years .Thereafter fertility rate declines.
- Other factors includes: cigarette smoking ,illicit drug use and occupational and
environmental exposures.



Ovary
Tube
Cervix
Endometrium
Male




Ovulatory dysfuncon (15-20/0)
Hypothalamic (hypothalamic amenorrhea)
Pituitary
Prolactinoma
Hypopituitarism







Ovarian
Pcas
Premature ovarian failure
Luteal phase defect (poor follicle production, premature corpus luteurn failure,
failed uterine lining response to progesterone) poorly understood
Systemic diseases (thyroid, Cushing's syndrome, renal/hepatic failure)
Congenital (Turner syndrome, gonadal dysgenesis, or gonadotropin deficiency)
Stress, poor nutrition, excessive exercise (even in absence of amenorrhea)



Outflow tract abnormality:
Tubal factors (20-30%)
PID
adhesions (previous surgery, peritonitis, endometriosis)
ligation/occlusion (e.g. previous ectopic)
Uterine factors (<5%)
Congenital anomalies (e.g. prenatal DES exposure), bicornuate uterus, uterine septum
Intrauterine adhesions (e.g. Asherman's syndrome)
Infection (endometritis, pelvic TB)
Fibroids/polyps (particularly intrauterine)
Endometrial ablation
Cervical factors (5%)
Hostile or acidic cervical mucous
Anti-sperm antibodies
Structural defects (cone biopsies, laser, or cryotherapy)
Endometriosis
Mulple factors (30%)
unknown factors (10-15%)




Ovulatory
Day 3 FSH, LH, TSH, PRL +/- DHEA, free testosterone (if hirsute)
Day 21-23 serum progesterone
initiate basal body temperature monitoring (biphasic pattern)
postcoital test - evaluate mucus for clarity, pH, spinnoarkeit (rarel~' done)
Tubal factors
HSG (can be therapeutic - opens fallopian tube)
SHG
Laparoscopy with dye insufflation
Peritoneal /uterine factors
HSG/SHG, hysteroscopy
Other
karyotype






Education - ming of intercourse in relaon to ovulaon (from 2 days prior to 2 days following
presumed ovulation), every other day

Medical
Ovulation induction
Clomiphene citrate (Clomid) - ovulation induction via increased pituitary gonadotropins
Human menopausaf gonadotropin [HMG (PergonaFM)]
Urofollitropin (FSH [Metrodin])
Followed by -hCG for stimulation of ovum release

May add
bromocriptine (dopamine agonist) if increased prolactin
dexametnasone for women with hyperandrogenism
(pCaS, adult onset congenital adrenal hyperplasia), metfonnin (PCaS)
luteal phase progesterone supplementation tor luteal phase defect

Surgical/procedural
Tuboplasty
Lysis of adhesions
Artificial insemination
Sperm washing

IVF (in vitro fertilization)
Intrafallopian transfers:
GIFT (gamete intrafallopian transfer)
immediate transfer with sperm after oocyte retrieval
ZIFT (zygote intrafallopian transfer) - transfer aer 24 hour culture of oocyte and sperm
TET (tubal embryo transfer) - transfer aer >24 hour culture
lCSI (intracytoplasmic sperm injection)
lUl (intrauterine insemination)

Oocyte or sperm donors
NM (in vitro maturation)




When should investigations begin?

<35 years: aer 1year of trying to conceive
-35-40 years: aer >6 months
>40 years: immediately
Earlier if:
- History of PID
- History of infertility in previous relationship
- Prior pelvic surgery.
- Chemotherapy/radiation in either partner
- Recurrent pregnancy loss
- Moderate & severe endometriosis



varicocele (>40%)
cryptorchidism (-8%)
idiopathic (>20%)
immunologic (-3%)
obstruction (-15%)





semen analysis and culture
post-coital (Huhner) test


Ovarian Cancer

Prepared by: Wafaa Al-Ahmadi
Sources: Toronto Notes 2008 + Obstetrics & Gynecology At Glance + Obstetrics & Gynecology Recall


Ultrasound characteristics of benign vs. malignant ovarian tumors:
Benign Malignant
< 8-10 cm in diameter >10 cm in diameter
unilateral Bilateral
Cystic Solid elements (internal papillary structures/mural
nodules)
Uniloculated Mutiloculated
Thin septations Thick septations
No ascites Ascites

Epidemiology
Life me risk 1.4% (1/70).
In women > 50 years, more than 50% of ovarian tumor are malignant.
4th leading cause of cancer death in women.
56% epithelial; 35% non-epithelial.
5-10 % of epithelial ovarian cancers have hereditary predisposion.

Risk factors
Nulliparity.
Early menarche/late menopause.
Age
Family history
Race Caucasian

Protective factors
OPC possibly because of ovulation suppression.
Pregnancy/breastfeeding.
Tubal ligation.
Hysterectomy.

Clinical features
Usually asymptomatic until disseminated.
Most present as stage III disease (advanced).
Early:
Post menopausal bleeding; irregular menses if pre-menopausal (rare).
Vague abdominal symptoms (nausea, bloating, dyspepsia, anorexia, early satiety).
Late (due to mass effect):
Increased abdominal girth from ascites or tumor itself.
Urinary frequency.
Constipation.
Fluid wave.




Lower malignant potential tumor:
Often called borderline tumors.
About 15% of all epithelial type ovarian tumors.
Tumor cells display malignant characteristics histologically, but no invasion is identified.
Treated with surgery.
No proven benefits of chemotherapy.
Slow growing, excellent prognosis.
5 years survival > 99%.
Pregnancy, OCP, & breast feeding are found to be protective.

Stages of ovarian cancer




Epithelia
ovarian tumor
87-90%
Metastatic
ovarian cancer
4-8%
Sex cord
stromal
5-7%
Germ cell tumor
5-7\%
Classification
of ovarian
cancer
Prognosis: (5 years survival)
Stage I: 75-95%
Stage II: 45-65%
Stage III: 20-40%
Stage IV: 10-15%

Classification of ovarian cancer





















Epithelial ovarian cancer:
Origin
Arise from coelomic epithelium (i.e. the mesothelium).
This epithelium also give rise to peritoneum & the paramesonephric (mllerian duct), which
explains the histologic similarities between lesions of ovarian, peritoneum, & urogenital tract.
Types:
Serous (50-70%)
o 20-30 bilateral
Mucinous (10-15%)
o Rarely complicated by pseudomyxoma peritonei.
o Implants seed abdominal cavity & produce large quantities of mucous.
Endometroid
Undifferentiated
Clear cell
Age: the median age at diagnosis is 61 years.
Hereditary factors:
5-10% of ovarian cancer paent have a hereditary cancer syndrome (most commonly familial
breast ovarian cancer). Germline mutaon in the BRCA 1 or BRCA 2 gene account for the majority
of cases.
Germ cell tumors:
Origin:
Derived from primitive germ cells of the embryonic gonad.
The vast majority of germ cell tumors occur in young women.
Types:
Dysgerminomas:
o Are the most common type (50%).
o The median age at diagnosis is 17 years.
o Lactate dehydrogenase may be a useful tumor marker.
o Overall long-term survival is 85%.
Endodermal sinus tumors:
o Are the second most common type.
o Have elevated serum alpha-fetoprotein (AFP) levels.
o Median age at diagnosis is 19 years.
Embryonal carcinomas.
Choriocarcinoma.
Immature teratomas.

Sex cord stromal:
Origin:
Gonadal/stromal origin.
Have low grade malignancies & recurrence are very uncommon.
May occur at any age.
Types:
Granulose cell tumors:
o Are the most common type (70%).
o 95% are stage at diagnosis & unilateral.
o Estrogen producing feminization effects (precocious puberty, menorrhagia, post-
menopausal bleeding).
Sertoli-leyding tumors:
o Are rare & frequently presented with signs of hyperandrognism as its an androgen producing
tumor virilizating effects ( hirsutism, deep voice, recession of front hairline).

Metastatic ovarian cancer:
From GI tract, breast, endometrium, lymphoma.

Investigations
Bimanual examination.
Solid, irregular, fixed pelvic mass is suggestive of ovarian cancer.
Blood work: CA 125 for baseline, CBC, LFT, electrolytes, creanine.
Radiology: CXR, abdo-pelvic U/S, transvaginal U/S; CT or US to asses urinary tract.
Bone scan NOT indicated.


Try to rule out primary:
Occult blood: if positive endoscopy barium enema.
If gastric symptoms: gastroscopy upper GI series.
If abnormal vaginal bleeding: PAP smear & endometrial biopsy to rule out concurrent
endometrial or cervical cancer.
Mammogram.
Treatment
For epithelial ovarian tumors:
Primary therapy:
Complete surgical staging (peritoneal cytoplogicaly, abdominal exploration, total abdominal
hysterectomy (TAH), bilateral salpingo-oophorectomy (BSO), biopsy or smear of the diaphragm,
omentectomy, select pelvic & para-aortic lymphadenectomy) maximal tumor cytoreduction are
the cornerstone of primary treatment. The goal of the surgery is definitive diagnosis, accurate
staging, & removal of all gross disease.
Adjuvant therapy:
Platinum-based chemotherapy is generally recommended for all stage 1c & higher cases. Six cycle
of carboplatin & paclitaxel (Taxol

) are given unless the disease progression is recognized.


Patient follow up:
CA 125 level & scan may be used to monitor response to therapy. Theres no survival benefits for
patient to under go second-look lapratomy after chemotherapy.
Progressive or recurrent disease:
Paent with progressive disease during chemotherapy or who recur within 6 months should be
considered for investigational trials. Patients with a good initial clinical response who recur after
at least 12 months of clinical remission may benet from secondary debulking & treatment with
platinum-based chemotherapy.
Palliation:
Despite aggressive surgical resection & adjunctive therapy, most patient die within a few years
from small bowel obstruction & malnutrition caused by intraperitoneal tumor. Palliative therapy
(treatment aimed at temporary relief of symptoms but not cure) is a critical part of preterminal
care to maximize patient comfort.

For germ cell tumor:
Unilateral oophorectomy if the woman desires to preserve fertility, otherwise TAH/BSO &
complete surgical staging.

For six cord stromal tumor:
As for germ cell tumor.

Screening
- No effective method of mass screening.
- Routine CA-125 level measurement NOT recommended.
- Controversial in high risk group: starng age 30, transvaginal U/S & CA-125 (non consensus on
interval)
Familial ovarian cancer ( 1 rst degree relave aected, BRCA-1).
Other cancers (i.e. endometrial, breast, colon).
May recommended prophylacc bilateral oophorectomy aer age 35 years or when child
bearing is completed (BRCA-1 or BRCA-2 mutaon).



Cervical cancer
Prepared by: Wafaa Al-Ahmadi
Source: Toronto Notes 2008 + Obstetrics & Gynecology At glance + churchills pocketbook Obstetrics
& Gynecology + eMedicine website + Dr.Saits lecture + obstetrics & gynecology recall

Epidemiology
Average age of onset is 47 years

Etiology

At birth, vagina is lined with squamous epithelium; columnar epithelium lines only the endocervix &
the central area of the ectocervix (original squamocolumnar junction).
During puberty; estrogen stimulates eversion of a single columnar layer (ectopy), thus exposing it to
the acidic pH of the vagina, leading to metaplagia (columnar to squamous).
Metaplagic squamous epithelium covers the columnar epithelium & new squamocolumnar junction
is formed closer to the external os.
The transformation zone (TZ) is an area of squamous metaplagic located between the original & the
new squamocolumnar junction (figure below)



















The majority of dysplasia & cancers arise in the TZ of the cervix.
Must have active metaplagia & inducing agent to get dysplasia.

Risk factors
HPV infection:
high risk associated with types 16, 18
low risk associated with types 6, 11
multiple partners
other STIs (HSV, trichomonas, Chlamydia infections).
High risk male partners.
Smoking
Young age at first intercourse
Immunocompromise.
Low socioeconomic status
? OCP use

Pathogenesis
HPV infection cause mutaon to p53 cells grow in abnormal form dysplasia carcinoma
in situ (CIS) invasion.

Clinical presentation
Squamous cell carcinoma (SCC):
Exophytic, barrel-shaped tumor
Adenocarcinoma:
Endophytic, with barrel-shaped cervix.
Early:
Asymptomatic.
Discharge initially watery, becoming brown or red.
Post-coital bleeding.



Late:
80-90% present with bleeding either post-coital, post-menopausal or irregular bleeding.
Spontaneous irregular bleeding.
Pelvic or back pain.
It can invade the bladder and rectum directly.
Symptoms that can evolve, such as constipation, hematuria, fistula, and ureteral
obstruction with or without hydroureter or hydronephrosis, reflect local organ
involvement.
The triad of leg edema, pain, and hydronephrosis suggests pelvic wall involvement.
The common sites for distant metastasis include extrapelvic lymph nodes, liver, lung, and
bone.
Physical signs:
In patients with early-stage cervical cancer, physical examination findings can be relatively
normal.
As the disease progresses, the cervix may become abnormal in appearance, with gross
erosion, ulcer, or mass. These abnormalities can extend to the vagina.
Rectal examination may reveal an external mass or gross blood from tumor erosion.
Bimanual examination findings often reveal pelvic metastasis.
Leg edema suggests lymphatic/vascular obstruction from tumor.
If the disease involves the liver, some patients develop hepatomegaly.
Pulmonary metastasis usually is difficult to detect upon physical examination unless pleural
effusion or bronchial obstruction becomes apparent.
Histology
Almost 90% are squamous cell carcinoma.
About 10% are adenocarcinoma.
There are other possibilities. Adenosquamous has a worse prognosis than squamous cell.
Malignant melanoma, sarcoma, lymphoma & small cell carcinoma can all occur.





Deferential diagnosis
Cervicitis
Endometrial Carcinoma
Pelvic Inflammatory Disease
Uterine Cancer
Vaginitis
Vaginal cancer
Metastatic cancer to cervix (rare)

Cervical screening guidelines (PAP Smear)
Endocervical & exocervical cell sampling, TZ sampling.
False posives 5-10%, false negaves 10-40%.
Identifies squamous cell carcinoma, less reliable for adenocarcinoma.
All women: start screening at age 21, or 3 years aer onset of vaginal intercourse.
Women > 30 years: If 3 normal PAPs in a row, & no previous abnormal PAPs can get screening every
2-3 years (if adequate recall mechanism in place).
Women > 70 years If 3 normal PAPs in a row & NO abnormal PAPs in the last 10 years, can
discontinue screening.
Hysterectomy:
Total: discontinue screening if hysterectomy was for benign disease & NO Hx of cervical
dysplasia or HPV infection.
Subtotal: continue screening according to guidelines.
Exception to guidelines:
Immunocompromise (transplant, steroid, DES exposure).
HIV & high risk
Unscreened patient

























In Saudi Arabia: start screening 1 year aer marriage, if it was negave for 2 or 3 mes repeat it
every 2-3 years & connue that ll she aged 70 years (if she was at low risk) but (if she was at high
risk) continue screening forever.

Workup
A Papanicolaou test should be performed in every patient suggested to have a diagnosis of
cervical cancer.
Cervical biopsy provide definitive diagnosis & is easily performed if the patient has a visible
cervical tumor.
If an abnormal pap smear or routine examination raises suspicion of cervical cancer,
colposcopically directed biopsy may be helpful.





After the diagnosis is established, a complete blood cell count and serum chemistry for
renal and hepatic functions should be ordered to look for abnormalities from possible
metastatic disease.
Once the diagnosis is established, imaging studies are performed for staging purposes.
A routine chest radiograph should be obtained to help rule out pulmonary metastasis.CT
scan of the abdomen and pelvis is performed to look for metastasis in the liver, lymph
nodes, or other organs and to help rule out hydronephrosis/hydroureter.
In patients with bulky primary tumor, barium enema studies can be used to evaluate
extrinsic rectal compression from the cervical mass.
The use of positron emission tomography (PET) scan is now recommended for patients with
stage IB2.

Clinical staging
Stage Description
Ia Cancer is confined to the cervix & identified only microscopically with invasion up to
5.0 mm & wide to 7.0 mm.
Stage Ia-1: up to 3.0 mm depth & 7.0 mm width.
Stage Ia-2: 3.1-5.0 mm depth & up to 7.0 mm width.
Ib Cancer is conned to the cervix & larger than stage 1a-2 OR associated with a visible
lesion.
Stage Ib-1: up to 4.0 cm cervical tumor diameter.
Stage Ib-2: > 4.0 cm cervical tumor diameter.
IIa Involvement of the upper 2/3 of the vagina, but no evidence of parametrial
involvement.
IIb Infiltration of the parametria but not out to the sidewall.
IIIa Involvement of the lower 1/3 of the vagina but not out to the pelvic sidewall if the
parametria are involved
IIIb Extension to the pelvic sidewall &/or hydronephrosis or non-functional kidney
(unless known to be attributable to other causes).
IVa Extension outside the reproductive tract with involvement of the mucosa of the
bladder.
IVb Distant metastases
Cervical cancer prognosis (5 years survival gures):
Stage I: 85-90%
Stage II: 60-75%
Stage III: 35-45%
Stage IV: 15-20%

Q: What colposcopic findings are suggestive of cervical cancer?
A: 1) Abnormally branched, looped, or punctuated blood vessels (secondary to
neovascularization of the tumoe & distortion of the blood vessels by the growing mass).
2) Abnormal appearance of the surface of the cervix.



Treatment
Primary therapy:
Stage Ia-1: may be treated with cone biopsy or simple hysterectomy.
Early disease (stage Ia-2 to IIa): may be treated with radical hysterectomy or radiation
therapy depend on patient age & medical status.
Advanced disease (stage IIb to IV): is treated by chemoradiation weekly cisplatine &
external beam radiation (teletherapy) followed by brachytherapy.
Adjuvant therapy:
Some patients with high-risk early stage or advanced disease may benefit from post-operative
radiotherapy or post radiation hysterectomy. Adjuvant therapy may decrease the risk of pelvic
recurrence, but a survival benefits has not been proven.
Recurrent disease:
Patient who develop recurrence after surgery alone are candidates for radiation therapy. Pelvic
exenteration (removal of bladder, uterus, rectum, & other involved structures) is indicated of
post-radiation recurrence with central pelvic disease. Unfortunately, the prognosis for patient
with recurrent cervical cancer is overwhelmingly poor.
Palliation:
Cisplatin or regional radiotherapy may be effective in reducing pain symptoms.

Prophylactic vaccine
Virus neutralization antibodies to prevent infection
Generate anbodies in genital tract epithelium directed against the L1 and L2 capsid proteins
Commercial HPV Vaccines:
GSK vaccine (Harper 2004) for types 16/18(100% ecacy)
Merck vaccine (villa 2005) for types 6/11/16/18 ( 88% ecacy (RCT PLACEBO)
0,1,6 months
16-23 y old
Gardasil: Quadrivalent HPV Vaccine:
0.5 ml IM, day 0, month 2, and month 6
COST ~$130 each vaccine dose
Storage: 2-8
o
C, should not be frozen, protect from light. (NEED TO PRESERVE THE ) COLD
CHAIN
Contraindications: hypersensitivity to the active substances or components
Precautions:
o May not be effective
o Not for use in active warts, cervical cancer, CIN VIN, VAIN
o Does not provide protection against none vaccine HPV types
o Not recommended for use in pregnancy, Category B



WHO:
Women 9-26
Do not need to have pap smear before vaccination
Testing for HPV is not recommended prior to vaccination
Sexually active women can be vaccinated, may be less effective in women
who have been previously exposed to HPV
Gestational Trophoblastic Disease-GTD



Definition
It is a spectrum of abnormal proliferation of trophoblastic associated with pregnancy

Classification
GTD classify to:
- benign --- Hydatiform mole
- malignant --- Gestational Trophoblastic Neoplasm (GTT)



PSTT = placental site trophoblastic tumor


Hydatidiform moles

Incidence
o Japan has highest incidence 2/1000 pregnancy
o Europe & north America 0.6 1.1 pregnancy


Types
o Partial &
o Complete

GTD
Hydatiform mole

GTT
Complete mole
Partial mole
Invasive mole PSTT Choriocarcinoma
Non-Metastatic metastatic
Low Risk
High Risk
Prepared by: Salman Jan
Sources: Toronto Notes + Tarek Arab sheet


- Chromosomal origin:



- Complete Vs. Partial:

Patrial Complete
o Age: > 40 y
o Hx. Of previous molar pregnancy
o Hx. Of recurrent abortion
o If mother blood group >> A &
father blood group O & vice versa

o 5-10% risk to transform into
carcinoma "less than complete
mole"
o Age: more common < 20y - > 40 y
o Race: more among Chaises,
Indian & far east. Less in white ppl
o Hx. Of previous molar pregnancy
o Diets: low in Beat-carotene
o Vit. A deficiency

o 20% risk to transform into
carcinoma
Risk factors
o Some of chorionic villi are swollen
& some are normal
o Contain some fetal blood vessels
in chorionic villi
o Hyperplasia in only
synsetiotrophblast
o Fetus can be seen or fetal
membrane or fetal parts
o All chorionic villi are swollen
o Absent of fetal blood vessel in
chorionic villi
o Hyperplasia in all trophoblast
(synsetiotrophoblast
cytotrophblast)
o Complete absence of fetus of
fetal membrane or fetal parts
Pathological
characteristic
o Abnormal vaginal bleeding during
pregnancy
o Hx. Of passing vesicles
o Sever nausea & vomiting
o Lower abdominal pain
o Pre-eclampsia symptoms "clinical
triad: HTN, proteinuria & non-
pitting edema"
o Hyperthyroidism
o Hx. Of IUGR & abortion
o Abnormal vaginal bleeding during
pregnancy
o Hx. Of passing vesicles
o Sever nausea & vomiting
o Lower abdominal pain
o Pre-eclampsia symptoms "clinical
triad: HTN, proteinuria & non-
pitting edema"
o Hyperthyroidism
Clinical Pictures
o small of date
o Vaginal Ex. >>> passage of
vesicles
o Pre-eclampsia
o Hyperthyroidism
o Ovarian cysts rare
o Fetal parts
o Large of date
o Ovarian cysts
o Absent of fetal movement
o Absent of fetal parts
o Vaginal Ex. >>> passage of
vesicles
o Pre-eclampsia
o Hyperthyroidism
Signs


Investigation
o U/S "diagnostic"
If complete: no fetus "snow storm appearance due to swelling of villi"
If partial: molar degenerative of placenta with developing fetus/fetal parts,
multiple echogenic regions corresponding to hydropic villi, & focal intra-
uterine hemorrhage
o BhCG
If complete: abnormally higher than 80000 mlU/ml
If partial: not very hight
o


Treatment
o suction evacuation followed by curettage & follow up:
o admin oxytocin during curettage to stimulate uterine contravtion
o BhCG level should steadily decline aer evacuaon to undetected level by 16 week, if
it still rise, think of either recurrence or pregnancy
o if recurrent after evacuation, chemotherapy required, the drug used is Methotrexate


Follow up
o contraception to avoid pregnancy during follow up period
o monitor BhCG level weekly after evacuation until Ve x 3 (usually takes 3-10 week)
then monthly for 6 months prior to trying conceive again
o if BhCG increased >> pt need chemotherapy



Notes:
o Physiology of B-hCG:
BhCG detected in blood 8 days aer ferlizaon
BhCG detected in urine 8-10 days aer missed abortion
Boubling me is 48h
In 1
st
10 w >> it duplicate in amount
10 20 w >> silght decline
20 w delivery >> same level

o Features of molar pregnancy at hight risk of persistent GTT:
Local uterine invasion as hight as 31%
BhCG > 100000
Excessive uterine size
Prominent theca-lutein cysts

o With developing of HTN in early pregnancy (< 20 w) think about GTD


Gestational Trophoblastic Tumors (GTT)

types
o choriocarcinoma
metastatic
non-metastatic
o PSTT
o Invasive moles

- Invasive Mole
o Diagnosis made by rising or a plateau in BhCG development of metastases following
treatment of documented molar pregnancy
o Histology molar tissue
o Invade locally >>> myometrium, serosa & vagina
o Metastases are rare
o Management: hysterevtomy, don't respond to chemotherapy


- PSTT:
o Occur in plasental site
o Tumor marker is HPL
o Can metastasis
o Rare aggressive form of choricarcinoma
o Abnormal growth of intermediate trophoblastic cells
o Low BhCG, production of hPL, insensitive to chemotherapy
o Poorly respond to chemotherapy
o Management: hysterectomy but inmetastasis (hysterectomy + chemotherapy)

- Choricacinoma:
o Often present with symptoms from metastases
o Highly anaplastic, highly vascular
o Can occur as primary ovarian tumor
o May follow molar pregnancy, abortion, ectopic or normal pregnancy
50% occur aer molar pregnancy
25% occur aer normal pregnancy
25% occur aer aboron or ectopic pregnancy

o Risk factor:
Hx. Of hydatidiform mole
Spontaneous abortion / ectopic pregnancy
Age: > 40 y
Blood type A
OCP long-term use

o Pathological characteristic:
Abnormal cyto & synsetio trophoblast
Absent of chorionic villi, elements of syncytiotrophoblast & cytrophoblast >>>
pathognomic
Necrosis & hemorrhage

o Non-metastatic >>> confined to uterus
o Metastac >>> 80% to lung then to other sites " vagian, liver, brain, ovary . Etc"

o Characteristic of low risk:
Duraon of disease 3 or 4 monthes
BhCG less than 40000 mlU/ml
No Hx. of previous chemotherapy
Metastatic to lung only

o Characteristic of high risk:
Duraon of disease more than 3 or 4 monthes
Level of BhCG more than 40000 mlU/ml
Hx. Of previous chemotherapy
Metastases to lung + liver vagina, brain ,,,, etc

o Clinical pictures:
Abnormal bleeding
Secondary post partum hemorrhage
Abortion
Ectopic pregnancy





-
Ovulation, Fertilization, Implantation and the Placenta
Prepared by: Ayah M Boudal, Nedaa bhkali
Source: Tarek Arab sheets


Primordial germ cell appears in the human embryo yolk sac at the end of 3
rd
week development.
Migration takes place from the yolk sac to the developing gonads.
Primordial germ dells differentiate, forming oogonia in the gonads. These are surrounded by a flat
layer of follicular cells.
Some differentiate into primary oocytes, which
then replicate DNA and enter prophase of the
first meiotic division.
Primordial follicle: primary oocyte plus surrounding
epithelial cells.




Near birth, primary oocytes are in the diplotene stage (resting stage during prophase) .
They stay in this stage unl puberty. 400,000 are
present at puberty, but only 500 are ovulated.
At puberty, 5-15 primordial follicles develop with each
cycle.
Primary oocyte (follicular cells change to granulose
cells) goes on to form the primary follicle. The
development of theca folliculi,zona pellucid and
thecae (interna and externa) then take place.
Antrum formation results in the secondary follicle
being formed, as well as the cumulus oophorus.


Graafian follicle: Mature follicle 10 mm or more in diameter
Surrounded by theca interna (steroid secretion rich in blood vesseles) and the theca externa ,
that merges with the ovarian stroma.

Before ovulation: Primary oocyte resumes 1
st
meioc division, resulng in 2 daughter cells (haploid),
these are the secondary oocyte and first polar body .
A second division (NOT THE SECOND MEIOTIC DIVISION) then takes place without DNA replication.
When secondary oocyte shows spindle formation, ovulation takes place.






Definition: the physical act of rupture of
the follicle, with release of the oocyte.

This is initiated by a surge of LH.
Oestrogen itself peaks before ovulation.

The secondary oocyte plus granulose cells
of cumulus oophorus are extruded.
At this point the secondary oocyte has
started its 2
nd
meiotic division.
Diagnosis of ovulation :
Occurrence of pregnancy
Retrieval of oocyte from the peritoneal cavity

History:
A history of regular cycles with pre-
menstrual symptoms + midcycle pain
indicates ovulaon in 90-95% of cases.
Basic body temp chart
This is a biphasic record that highly
correlates with ovulation.
In the first half of the cycle it will be low,
then a rise occurs.
If conception does not occur , temperature
drops to the previous level.







Cervical mucus
Secretory phase: scanty, thick, cloudy, highly cellular
At ovulation: watery, copious, clear, acellular


Ultra sound
The size of the follicle prior to rupture is 18-20mm, thus a decrease in size would indicate whether ovulation
had occurred or not.

Endocrine tests
Surge of oestradiol and LH prior to ovulation
Day 21 , progesterone level exceeds 5 nanograms
Presumptive evidence of ovulation:
BBT
Ultrasound changes
Endometrial biopsy
Proliferative phase specimens will vary, however during the period between ovulation and menstruation
i.e. day 14 and day 28 samples will be the same. Thus take a sample at this me and date the endometrium.




Occurs in ampullary region of uterine tube.
Doses NOT need the zona reaction or c apacitation to occure.
Capacitation : period of conditioning in female genital tract, lasng 7 hrs and
involving the removal of the glycoprotein coat and seminal plasma proteins
from the acrosomal region.
Acrosome reaction ( zona reaction ): Enzymes released, allowing penetration of the zona pellucid . It occurs
after binding to zona pellucid.
Fertilization involves:
Penetration of the corona radiate
Penetration of the zona pellucid
Fusion of the oocyte and sperm cell membranes
The oocyte finishes the second meiotic division when the spermatozoa enters it .
Cleavage
Fusion---zygote---blastomeres---3
rd
division formation of compacted embryo---division to 16 cell morula---
32 cell balstocyst
Inner cells: give rise to embryo
Outer cells: trophoblast
Fertilizable life span : Egg: 12-24 hrs
Sperm: 72 hrs

Zona pellucid : This is species specific , and is
the site for the zona reaction
Zona reaction : Hardening of the zona and
inactivation of receptors







Implantation: The uterus is in the secretory phase , thus consists of 3 layers,
the compact layer, spongy layer and basal layer .
The ferlized ovum reaches the posterior uterine wall 3 days aer ferlizaon
(when it has reached the morula stage), and becomes embedded between the
opening of the glands, The Zona is shed before this.







At the time of implantation, HCG can be detected in the maternal ser um
HCG the maintains corpus luteum for 6-8 weeks, and therefore pregnancy, unl progesterone
production is shifted to the placenta
The endometrium , under the influence of oestrogen , progesterone , IGF-1. PGE2 and
plasminogen acvator,reaches 10-14 mm in thickness at the me of implantaon.

It takes 4 days to traverse the fallopian tube , the site of implantaon is the
upper posterior uterine wall in the mid saggital plane.

Initially the wall of the blastocyst is facing the uterus lumen, and consists of a single layer of cells.
Opposite wall : consists of trophoblast and inner cell mass (the embryonic disk) which gives rise to the
dorsal ectoderm and ventral endoderm

Early stage of implantation
Development
The trophoblast forms, and has an inner layer of cytotrophoblast and outer layer of synctiotrophoblast.
Between 10-13 days POST OVULATION lacunae appear in trophoblast cell mass
These form inter-villous spaces
which be filled by maternal
blood
Progesterone causes the
endometrium to thicken
Deciduas basalis :directly beneath site
of implantation
Deciduas capsularis : overlying
developing ovum and separate form
the uterine cavity
Deciduas vera : remaining lining of
uterine cavity








The decidua is the functional part of the placenta and is shed during parturition
Trophoblast strands branch to form
villi traversing lacunae
Embryonic mesenchyme appears, within the cavity of blastocyst, and when lined by mesoderm
becomes the extraembryonic coelom
On 17
th
day both maternal and foetal blood is functional and the placental circulation is established ,
being completed when the embryonic blood vessels are connected to chorionic blood vessels
The greater part of the chorion id known as the (levae).
Aer 3
rd
month, it is in contact with the amnion, prior to which they were separated by the
extraembryonic coelomic cavity
16-20 wks, the levae fuses with deciduas vera , and most of the uterine cavity is obliterated
The placenta
Full term placenta
Discoid
Diameter : 15-25 cm
500-600 g in weight
15-20 cotyledons on maternal
side
At 4
th
month, the placenta has 2 components:
Foetal component formed by chorion
frondsum
Maternal component formed by deciduas
basalis
The deciduas forms the decidual septum ,thus dividing placenta into cotyledons

The foetal cotyledons constitute the functional unit of the placenta
Each cotyledon contains a primary villus stem arising from the chorionic plate which is
supplied by the primary branches of the foetal blood vessels
The primary stem is divided into secondary and tertiary stems which arise from the terminal villus.
The terminal villi are the site of maternal- foetal exchange
Placental circulation :
Spinal arteries,(80-100) pierce the
decidual plate , cau se blood to bathe
the villi of the villous tree. Inter-villous
spaces contain 150 ml blood , and are
replenished 3-4 mes per minute
Placental membrane : separate maternal
and foetal blood and has 4 layers :
Endothelial lining of foetal vessels
Connective tissue of villous core
Cytotrophoblastic layer
Syncytium
Functions of the placenta :
Gas exchange and oxygenation of foetal blood
Exchange of nutrients
Trans mission of maternal antibodies (IgG)
Hormone production
(Progesterone,Oestriol,hCG,
somatomammotropin)
Variations in placenta
Bipartite /tripartite : vessels cross between
incompletely divided lobes
Duplex/triplex : opposite of the above
Placenta succenturiata : blood vessels connect accessory lobes to main placenta ,
and result in compression of blood vessels or rupture at birth
Velementous insertion: result in compression of blood vessels or rupture at birth
Placenta circumvallata : Circular depression on foetal surface of placenta.
Amnion and chorion folded back on themselves.
Regression of villi development.

Incidence of abortion in early pregnancy and bleeding in late pregnancy increased.
Placenta membranacea: persistence of villi of chorion levae as well as frondsum, producing a third placenta that
surrounds the foetal membranes . Separation and expulsion may be incomplete during
S3 labour.
Amniotic fluid :
Function :
Allows foetus room for growth and movement
Protective , contains antibacterial activity
Aids dilatation of cervix in labour
May serve as means of communication
Without it,the uterus would compress the foetus when it undergoes
Absence of adequate amounts during mid pregnancy are associated with pulmonary hypoplasia at birth.
Arises from :
1
st
trimester : Ultrafiltrate of maternal plasma
Later : Transudation of foetal plasma across the foetal skin
12-24
th
week: Foetal urine contributes to it
Other sources : Foetal secretion from the GIT and respiratory tract and transudate across the
umbilical cord
At term , 700-1000 ml of amnioc uid is exchanged every 24 hrs
Oligohydramnios :
Marked deficiency in volume of amniotic fluid
May produce foetal hypoxia
Associated with intrauterine growth retardaon in 60% cases
Polyhydramnios :
Excessive volume , usually exceeding 2 L
Complications include :
Increased risk of premature labour
Maternal respiratory discomfort
Umbilical cord prolapse at time of rupture of membranes
Fetal malpersentation
Diabetes Mellitus during Pregnancy
Prepared by: M. Bokhary 6
th
year student - 2008
Sources: TN 2007 Baby pink sheets Clinical sessions



1. Frank Diabetes : DM developed before pregnancy (Either type I or type II)
2. Gestational DM (GDM) : onset of diabetes during pregnancy




1. DM I : no insulin due to pancreatic damage - require external insulin -
2. DM II : insulin resistance - require life style modification & OHG -
3. GDM : imbalance between maternal insulin & placental hPL

As the fetus grows, it require increasing glucose demand. By week 24-28, the placenta secretes Hpl -
human placental lactogen- . This hormone rises the blood glucose levels (i.e. diabetogenic). As a response,
maternal insulin levels will rise to maintain the maternal glucose levels within normal. IF the maternal
pancreatic function is not sufficient to counter the increasing levels of hPL, GDM will occur.





1. Up to : 4%
2. MOST COMMON medical complications during pregnancy
3. Do we routinely screen for GDM ? NO! screen only if there is a RISK FACTOR using GTT.
low risk (no known risk factors) : you CAN screen using GCT.



What are the risk factors for GDM (when do we screen for GDM) ?

Maternal History Past Pregnancy History Current Pregnancy History
1. Family Hx of DM
2. Past Hx of GDM
3. Age extremes : <20 & >35
4. Obesity
5. Mutiparity
6. Hx of Recurrent abortion
7. Hx of unexplained IUFD
8. Hx of Anomalies
9. Hx of Macrosomia

10. Persistent GlucosUria
11. PolyHydramenious
12. Fetus large-for-date
13. Hx of Macrosomia






1. S/S of DM : thirst, polyphagia, increased Wt gain, polyuria (hard to distinguish cause its a pregnancy
symptom)
2. Fetus is BIG-FOR-DATE


GDM definition is:
NOT related to specic date e.g. aer 20 weeks
NOT related to Persist/not persist after
pregnancy
Maternal insulin is rising, wouldnt the fetal have hypoglycemia ?
Answer is : NO, maternal insulin does not cross placenta
IUGR is NOT an indication for Screening




I am suspecting my patient to have GDM .. how to diagnose ?

1. Low risk ? do GCT (Glucose challenge test)
How to do ?
o Pregnancy is at week 24 (maximum insulin resistance & starng hPL)
o Paent takes 50g glucose (no need to fast)
o Record glucose level aer 1 hour

If more than 7.8 mmol (140 mg/dl),the test is +VE, proceed to GTT.


2. High risk ? go for GTT (Glucose tolerance test) skip GCT:
How to do ?
o Do it in 1
st
Ante-natal visit. If normal, repeat at week 24
o Paent takes 100g glucose
o 12 hours fasng no smoking & caeine of 3 days
o Record glucose level at (fasng), (aer 1 hour), (aer 2 hours), (aer 3 hours),

Normal readings (OSullvian criteria) no more than :
o Fasting : 5.8 mmol (105 mg)
o Aer 1 h: 10.6 mmol (190 mg)
o Aer 2 h: 9.2 mmol (165 mg)
o Aer 3 h: 8.1 mmol (145 mg)

Abnormal readings !
o 1 reading abnormal : impaired GTT = paent is high risk to develop GDM
o 2 readings abnormal : paent has GDM




What kind of COMPLICATIONS might happen if my patient has un controlled DM ?
They are the complicaons results from (1) Hyperglycemia, (2) fetal hyper insulinemia

Early
Conception
1st Trimester
2nd & 3rd
Trimester
In labor Neonatal
Maternal
specific
1. Congenital
Anomalies
2. Abortion

Mainly DM I
unlikely if
GDM
1. PolyHydraminious
2. Mal Position &
Presentation
3. Abnormal
placenta
implantation
1. Macrosomia
2. PROM
1. Sholder
dystocia
2. PPH
3. Cesarean
Section
1. Hypoglycemia
2. RDS
3. Neonatal
Jundice
4. Kernictrus
1. 50%
Develop
DM II
later in life
2. Complicati
on of DM







Congenital anomalies:
most common : cardiac anomalies
most specific : caudal regression
Explanation of complication :

Complications :

:
Hyperglycemia embryogenesis . Congenital Anomalies !
Abortion .
.. :

1
st
Trimester : :: :
Fetal polyuria PolyHydraminious
PolyHydraminious Mal Position & Presentation
Abnormal Presentation Abnormal placenta implantation = Previa

2
nd
& 3
rd
Trimester : :: :
Hyperglycemia fetal hyper-insulinemia Macrosomia
PloyHydraminious Macrosomia uterine-over-distention PROM

During Labor : :: :
uterine-over-distention Uterine Atony = PPH
Macrosomia Sholder dystocia hypoxia brain
damage
Mal Position & Presentation Higher Incidence of Cesarean
Section

Neonatal period :
fetal hyper-insulinemia Neonatal Hypoglycemia
Hyperglycemia Delayed organ maturation
:
- RDS : Delayed lung maturity
- Neonatal Jundice : Delayed liver enzymes maturity
- Jaundice Kernictrus ! .





Whatever type of DM, our goal is achieve STRICT NORMOGLYCEMIA
unlike Medicine, we do not accept normal range. Glucose level must be strict

The more restricted glucose, the more normal the pregnancy will be.
4 things to keep in mind:
1. Monitor maternal blood-sugar profile.
2. Monitor fetal well-being.
3. Decide Timing of delivery.
4. Follow up after delivery.

3 Key factors in management:
1. Education: to assure compliance! Nature of disease, complications, how to monitor.
2. Diet & exercise
3. Insulin

Maternal blood-sugar profile
o HB
A1C
: during first visit.
o Stop OHG drugs : they cross placenta (teratogenic & fetal hypoglycemia)
o Normal diet for any pregnant women = 1800 kcal/day (36kcal/kg/day)
o Advise patient to have glucometer (monitor blood glucose daily).

o For follow up during visits : do 2 Point test
What is 2 Point test ?
Paent fast for 8 hourse (mid night)
In the morning (8 AM) tell patient to come & bring her breakfast.
Take blood glucose @ fasng, and 2 hours post prandial.
Normal values: no more than : (5.5 mmol fasng) & (6.6 mmol post prandial)
Normal results ? follow up again aer 2 weeks.
Abnormal ? do : 4 point test

o follow up using 4 Point test
What is 4 Point test ?
Admit patient, make her NPO starting midnight.
In the morning (8 AM) take fasting blood sugar.
Take blood glucose 2 hours post prandial of breakfast, lunch, dinner.
You decide the diet, not her own diet.
Normal values: no more than : (5.5 mmol fasng) & (6.6 mmol post prandial
any meal)
Normal results ? educate for more diet restriction and consider Insulin.
Abnormal ? Go for Insulin

o Insulin
Dose correction:
1
st
Trimester : 0.6 units x ideal weight
2
nd
Trimester : 0.7 units x ideal weight
3
rd
Trimester : 0.8 units x ideal weight

How to give ?
2/3 of the dose: AM (1/3 regular & 2/3 NPH)
1/3 of the dose: PM (1/2 regular & 1/2 NPH)

Fetal Well-being:
o BPP & NST.
o < 36 weeks : once every 2 weeks
o > 36 weeks : Weekly


Timing of Delivery:
o Controlled ? wait ll spontaneous onset /or Induce by 40 W.
o Uncontrolled ? wait for lung maturity (38 w) and induce


Follow up after delivery:
o After delivery, insulin requirement dramatically drop
o If Glucose level >8 mmol, use 2/3 of pre-pregnancy insulin dose.
o DM I : No insulin required during next 38-72 h
o 6 weeks post-partum : repeat GTT.
Normal ? it was GDM
Abnormal ? it is frank DM
Renal Disease in Pregnancy

Prepared by: Elham Algethami
Reference: Hacker + Tarek Arab + emedicine.com


Normally, renal blood flow and GFR in pregnant woman increase 40% above the non pregnant levels.

UTI:
Due to dilation in collecting ducts and ureters lead to stasis in urine.

Asymptomatic bacteriuria

Large numbers of bacteria are present in the urine, but the patient has no symptoms of a urinary
tract infection
* (>100,000 colonies/ml of a single organism in a clean-catch sample of urine ).

Incidence: 2-7% imp
Causative organism:
E.coli (80-85%)>> hacker
Klepsiella
Proteous
Enterobacter sp.
- Up to 30% of paents develop pyelonephris if asymptomac bacteriuria is le untreated.
- Treatment with a 10-day course of oral antibiotics is warranted and reduces the incidence of
pyelonephris to approximately 3%.

Effective therapies include nitrofurantoin, ampicillin, amoxicillin, or sulfonamides.
Urinalysis with culture should be performed and evaluated on a monthly basis after resolution.

Cystitis
- Cystitis is associated with symptoms of dysuria, urgency, and frequency, usually without
systemic signs.

- Keep in mind that symptoms of cystitis and pyuria accompanied by a "sterile" urine culture
finding may be the consequence of urethritis caused by Chlamydia trachomatis, a common
pathogen of the genitourinary tract.

- Mucopurulent cervicitis usually coexists, and erythromycin therapy may be effective.
- Aggressively treat cystitis with oral antibiotic regimens.

Pyelonephritis
- Pyelonephris, a bacterial infecon of the kidneys, occurs in up to 2% of pregnant women.
- Onset is usually abrupt and is characterized by fevers, chills, flank pain, anorexia, nausea, and
vomiting. Costovertebral tenderness can usually be elicited by physical examination.
- The most likely etiologic organisms include Escherichia coli and Klebsiella, Enterobacter, and
Proteus species.

- Up to 15% of paents have concurrent bacteremia.
- Complications other than bacteremia include hemolysis, sepsis, and adult respiratory distress
syndrome ( why ? because it secretes endotoxin mediated alveolar injury and hemolysis ), and
death.

- Effect on mother and fetus preterm labour , fetal death , IUGR..
Investigation:
Urine analysis >> WBCS is high, bacteriuria .
Urine culture>> +ve ..
Urine leukocyte estrase and nitrate is +ve .
Blood creatinine >> decreased.
Management:
Pyelonephritis requires hospitalization and administration of intravenous antibiotics and
intravenous fluid administration.
Continue treatment with intravenous antibiotics until fever resolves.
Effective regimens include ampicillin plus gentamicin or a third-generation cephalosporin.
Continue oral administration of antibiotics and suppressive therapy throughout the pregnancy.

Acute renal failure

There are peaks in the first trimester (related to unregulated and/or septic abortion) and the late
third trimester (related to obstetric complications).

Causes:
Prerenal ( pt came with hx of fluid or blood loss)
Hemorrhage
Volume depletion from GI or renal losses, burns, fluid sequestration, or low cardiac output states
(eg, chronic heart failure and other diseases of myocardium, valvulopathy, arrhythmia, pericardial
diseases, tamponade)
Systemic vasodilation (eg, sepsis, anaphylaxis)
Disseminated intravascular coagulation
Renal (interstitial)
Acute tubular necrosis most common cause.
Postrenal
Less common pt with kidney stone it less than .03 % of pregnancies.

Investigations:
Renal studies
Urine output oliguria ( less than 25 mL/ hour)
BUN to creatinine rao 20:1
But the BUN and creatinine is decreased
Fractional excretion of sodium = FENa : urine Na /plasmaNa/urine Cr/plasma Cr 100.. less than
1% >> hypovolemia .
more than 3%>>tubular damage
Urine osmolality > 500 mOsm/L







Cardiovascular studies:
Swan Ganz catheter monitor Lt and Rt ventricular filling pressures, COP, PCWP

Urologic studies:
Foley catheter and renal sonogram obstructive causes.

TTT:
According to cause.

Chronic renal failure

- Mild renal insuciency (serum creanine level, <1.5 mg/dL)
- Moderate renal insufficiency (serum creanine level, 1.5-2.4 mg/dL) progressed to ESRD
- Severe renal insuciency (serum creanine level, >2.5 mg/dL) progressed to ESRD.

Effect on Mother and Fetus:
SGA infants, preterm labor, and stillbirth

TTT:
As a case of ARF.
FH monitoring and U/S IUGR.
And start dialysis.
During hemodialysis, follow uterine and fetal monitoring and make every attempt to avoid
dialysis-induced hypotension
Place the patient on a transplant list.
Bleeding in 3
rd
Trimester (Antepartum Hemorrhage)
Prepared by: Sameerah Albugami 6
th
year medical student (completed by Wafaa Al-Ahmadi)
Source: Hacker + Toronto notes 2008 + Obstetrics & Gynecological Recall + Tarek Arabs sheets.



Bleeding at third trimester or vaginal bleeding from 20 weeks to term.
Incidence: 4%



Placental Uterine Cervical Vaginal Bleeding tendency
Placenta previa Cervivitis Trauma Clotting disorders
Placenta abruption Cervical erosion
Vasa pravia
Uterine rupture

Cervical Ca
Infection Heparin



Definitions:
Abnormal insertion of placenta in lower uterine segment (covering or near to the internal os).

Types: complete , marginal or partial.
- Complete: placenta completely covers internal os (grade 4).
- Partial: placenta parally cover internal os (grade 3).
- Marginal: edge of the placenta extend to the margin of internal os (grade 2).

Incidence: 0.5%
Etiology: Idiopathic.
Risk factors:
1) Increase maternal age.
2) Multiparity.
3) Past Hx of placenta previa.
4) Multiple gestation.
5) Previous C/S OR scars (myomectory..etc).
6) Uterine tumors or anomalies.

Pathopyhysiology:
Bleeding occur as a result of the disruption of the placental attachment secondary to the
development & thinning of the uterine lower segment in the 3
rd
trimester.

Presentations:
History:
- Painless bright red vaginal bleeding in the 3
rd
trimester.
- Remember that: sudden, causeless, painless and recurrent or post coital (in previously normal
pregnancy).
- Degree of hypovolaemia & shock that present corresponds to the apparent blood loss.
Physical examination:
- Do NOT perform a vaginal examination until placenta previa has been ruled out by U/S.
- The uterus is soft and non tender.


low lying placenta is not placenta previa (in the low
lying placenta; the placenta reaches the lower uterine
segment & within 2 cm of the internal os.

Q. What is the first episode of bleeding called?
A. The sentinel bleeding, usually ceases spontaneously but always
recurs. It usually occur at 29-30 weeks gestaon.

Complications:
Fetal:
1-perinatal mortality.
2-prematurity.
3-IUGR ??
4-fetal mal-presentation (breech & transfers lie are common).
5-PROM.
6-congenital anomalies.
Maternal:
1-maternal mortality.
2-post-partum hemorrhage and hypovolaemic shock ,anemia and acute renal failure.
3-sheehan syndrome.
4-placenta accereta.
5-hysterectomy.

Investigations: U/S diagnosis .

Management:
1) Stabilize the patient: large IV with hydration & O
2
.
2) Maternal Monitoring vital signs, CBC (for degree of bleeding), urine output,
coagulation profile.
3) Fetal monitoring NST, BPP, U/S.
4) Cross matching 4 units & blood product available.
5) Give the mother rhogam if mother is RH negative.
6) If GA<37 weeks:
Excessive bleeding or fetal distress perform C/S regardless of the GA.
Minimal bleeding expectant management.
7) If GA>37 weeks and large bleeding delivery by C/S.










Definitions:
Premature separaon of normally implanted placenta aer 20 weeks gestaons.

Incidence: 0.5_1.5%
Etiology: Idiopathic
Risk factors:
Maternal:
1) Past Hx of abruption placenta.
2) Maternal hypertension.
3) Cigarette smoking.
4) Multiparity.
5) Increase maternal age.
6) Uterine anomalies ,fibroid
7) Trauma.
If the placenta is 2 cm from the
cervix; it is save to deliver vaginally.
'------- - -;-'~- ;)- ;~
In case of placenta previa, which type of C/S is performed?
lower transfers C/S except in case of highly vascular anterior placenta previa Dr.Smaa Nather said we will perform
high transfers C/S & never perform classical type, BUT Dr.Ramadani said we will perform classical type !!!


Fetal:
1) PROM.
2) Polyhydramnios.
3) Multiple gestation.

Pathophysiology:
Anomaly of spiral arterioles hemorrhage inside decidual basalis formation of decidual
hematoma result in separation of deciuda from basal plate predispose to further separation
& bleeding as well as compression & destruction of placenta tissue. Pain ensues as a result, as can
acute fetal distress.



Presentation:
1) Painful vaginal bleeding (blood loss does NOT reflect the severity of abruption because some
of the blood may not escape the uterus). The pain is sudden onset, constant , localize to lower
back and uterus.
2) Uterine tenderness (at the site of implantation).
3) Hyperactivity & increased tone, Uterine contractions.
4) Fetal distress or fetal demise may occur.






Presentation is divided into mild, moderate & sever:
Mild Moderate Sever
25% of placenta bed
separated
25-50% of placenta bed
separated
50% of placenta bed
separated
Abdominal pain Gradual Sudden
Mild tenderness on Ex Rigid, tender uterus Sever abdominal pain
Firm uterus Continuous, sever abdominal
pain
Moderate to absent bleeding
Minimal per vaginal loss Moderate to sever per
vaginal blood loss
Fetal distress/demise of
fetus
No fetal distress Fetal distress Maternal hypovolaemia,
shock, oligorrhea, DIC
Mother is stable


Complication:
Fetal:
1) Fetal distress.
2) Fetal death (35% perinatal mortality).
3) Prematurity & its complications.
4) IUGR.
5) Neurological sequale e.g. cerebral palsy.



Blood may dissect towards uterine fundus concealed hemorrhage.
OR extends downward towards cervix revealed hemorrhage. But
the most common is mixed

- 20% of bleeding cases are concealed & an increased fundal hight will give an indication of
further concealed bleeding.
- If mother is multiparous or in labor, there is a higher risk of amniotic fluid impolism.
- NEVER perform vaginal examination until placenta previa has been ruled out.


Maternal:
1) Maternal mortality.
2) DIC (20% of cases).
3) Acute renal failure.
4) Renal tubular acidosis.
5) Anemia.
6) Hemorrhagic shock.
7) Shehans syndrome.
8) Amoniotic fluid embolus.
9) Ischemic necrosis of the distant organs.
10) Couveliar uterus (purplish or bluish appearance of uterus at time of C/S. it is caused by
extravasation of blood into the uterine muscle & beneath serosa).

Investigations:
Most abruption are clinically diagnosed. U/S may show placenta clot, but usually is in only 2% of cases.

Management:
1) Admission
2) IVF, steroid if GA < 34 weeks.
3) Anti D in Rh ve women.
4) Correct maternal hypovolaemia.
5) Check for DIC.
6) U&E, CBC, clotting.
7) Establish fetal condition by CTG.
8) In case of mild abruption:
In preterm (<37 weeks) & no fetal distress give steroid, serial Hct to assess concealed
bleeding ,deliver when fetus is mature or hemorrhage dictates.
In term (> 37) prompt delivery {oxytocin (pitocin) augmentation preferred to C/S
unless theres fetal distress or maternal hemodynamic instability}
9) In case of moderate to sever abruption:
Vaginal delivery if no fetal distress
If theres fetal distress or materal hemodynamic instability deliver by C/S.
10) In case of dead fetus induce labor.



Comparison of hemorrhage from placenta previa with that from placenta abruption:
Placenta previa Placenta abruption
Painless Painful
No ppt factors ppt factor
Less distressed Agitated & distress
Soft abdomen Tenderness, tense abdomen
Abnormal lie & presentation Normal lie & presentation
Less likely abnormal CTG More likely abnormal CTG (hypoxia)
Random association/pre-eclampsia More marked association/pre-eclampsia
Coagulation defect later Coagulation defect sooner





Recurrence is 10% aer 1 abrupon ,
25% aer 2 abrupons.



Definition:
Unprotected fetal vessels pass over the cervical os associated with velamentous insertion of cord
into membranes of placenta or succenturiate lobe.

Incidence: 1in 5000 deliveries.
Clinical features:
Rupture of vasa may occur in labor or with PROM cause:
1) painless vaginal bleeding and fetal exsanguinations or death.
2) Tachycardic/bradycardic on CTG.

Investigations:
APT TEST:
Distinguish between fetal & maternal RBCs based on the marked resistance to pH changes in
fetal RBCs.
<NAOH>mixed with blood: If turn to pink fetal blood. If turn to yellow maternal blood
Wright stain on blood smear and look for nucleated red blood cells.

Management: Emergency C/S regardless the GA.

Bleeding is fetal, not maternal.. total fetal
blood is 330 ml !
every single ml is a disaster !

Miscarriage (Abortion)

Prepared by: Dalal Al-Omar

Definition
It is terminaon of a pregnancy before 20 weeks gestaonal age, or expulsion of fetal ssue (fetal
weight) < 500 gm.

Types of Abortion
Induced or Spontaneous .

Types of Spontaneous Abortion:-
1- Threatened abortion.
2- Inevitable abortion.
3- Incomplete abortion.
4- Complete abortion.
5- Missed abortion.
6- Recurrent aboron; 3 successive spontaneous aborons.












Predisposing Factors
1- Maternal Factors;
- the risk of abortion increases with maternal age.
- Medical disease; D.M., SLE & Hypothyroidism.
- Infection (Mycoplasma, Listeria or Toxoplasma).
- Smoking, Alcoholic.
- Sudden physical or emotional shock.
- Cervical Incompetence (the most common cause of aboron in 2
nd
trimester).

The diagnosis is usually made when a mid-trimester pregnancy is lost with a clinical picture of sudden
unexpected rupture of the membranes, followed by painless expulsion of the products of conception.
- Uterine Adhesion; synechiae or Asherman's $.
- Uterine Abnormalities; congenital or acquired (associated with pregnancy loss in both the 1
st
&
the 2
nd
trimester).

2- Fetal Factors; Severe congenital anomalies either Genetics or morphological anomalies.

3- Chromosomal Factors; (the most common cause of aboron in 1
st
trimester)
Either Genetics or Morphological Abnormalities .

4- Immunological Factor; as Rh-Incomatability.

Etiology of recurrent pregnancy loss
MAKE ME
1- Mechanical; Uterine anomalies, cervical incompetence.
2- Autoimmune; antiphospholipid antibody syndrome, lupus anticoagulant.
3- Karyotype; both parents.
4- Endocrine; DM, hypothyroidism.
5- Maternal infection.
6- Environment; smoking, alcohol, drugs, radiation.

Management of abortion
- Always rule out ectopic.
- Always check Rh status before D&C and give RoGAM when it's ve.
- Always ensure patient is hemodynamically stable.

Intrauterine Fetal Death (IUFD)
Prepared by: Wafaa Al-Ahmadi
Sources: Toronto Notes 2008 + Tarek S. Arab sheet + obstetrics & gynecology At Glance



Fetal death in uterus aer 20 weeks gestaon before onset of labour.

DO NOT be confused with:
Missed abortion: intrauterine fetal demise before 20 weeks gestaon with complete retenon
of products of conception.
Still birth: birth of fetus that shows no evidence of life (heart beat, respiration or independent
movement) at any me aer 24 week gestation.
Abortion: Unexplained, unplanned, spontaneous loss of a pregnancy before 20 weeks gestaon.
Can be dened as expulsion of fetal ssue < 500 g.

Incidence: 1% of pregnancies.



Idiopathic 50% of cases
Maternal:
HTN & pre-eclampsia
DM
Anti-phospholipid syndrome
Medical diseases
Infections
Fetal:
Congenital anomalies.
TORCH.
Vasa praevia.
Cord prolapsed.
Erythroblastosis foetalis.
Placenta:
Insufficiency




Decreased perception of fetal movement by mother.
Fetal heart & maternal weight are not increased.
Absent of fetal heart tone.



U/S:
Lack of fetal movement.
Absent of cardiac activity.
No growth (if previous U/S is available).


TORCH=Toxoplasmosis, Other infections
Rubella, CMV, Herpes simplex
Other infections= Hepatitis B, Syphilis,
Varicella-Zoster Virus, HIV
Negative beta-HCG does not rule out IUFD.





- Let the patient to choose either induction of labor or expectant management for spontaneous onset of
labor.
- Address psychological aspect of fetal loss including anxiety & depression.
- look for cause of death, risk of recurrence & counseling for future pregnancies.

1) Watchful expectancy:

Wait for labour to begin (up to 4 weeks).
If not go to induction of labour.
Monitor Hct, platelets, fibrinogen, PT/PTT weekly because of the risk of DIC.
If fibrinogen, platelets decrease & PT/PTT increases, delivery baby.
If bleeding occurs along with the above changes, give fresh frozen plasma & deliver.


2) Induction of labour:

a) 20-28
th
week:
20 mg q3hrs prostaglandin E2 suppository (vagina) OR misoprostol

Risks of prostaglandin E2:
Uterine rupture
Laceration

Side eects of prostaglandin E2:
Nausea, vomiting, diarrhea, pyrexia.

Contraindications:
Previous C/S, previous myomectomy, bronchial asthma, acute pulmonary disease.


b) > 28
th
week:
Oxytocin if no contractions & favorable bishops score
Smaller doses of E2 due to risk of uterine rupture
Laminaria to ripen cervix.














if the induction of the labour was contra-
indicated go to C/S


3) Post-partum: to determine the cause.

Investigation Reason
CBC Anemia, leucocytosis
Clotting screen DIC
Kleihauer test Foeto-maternal transfusion
Virology, infection screen CMV, parvovirus
Autoantibody screen SLE, antiphospholipid syndrome
Blood & placenta culture Infections e.g: Listeria, TORCH
Antibodies to Rh-negative women Hemolytic disease
Toxoplasma antibodies Toxoplasmosis
Skin biopsy/cardiac blood/placenta biopsy Chromosome analysis
Full X-ray or MRI ID congenital defects



10% risk of DIC.

Intrauterine Growth Restriction (IUGR)
Prepared by: Wafaa Al-Ahmadi
Sources: Obstetrics & Gynecology Recall + Toronto Notes 2008+ Obstetrics & Gynecology At Glance



(either small or large for date):
Incorrect date
Maternal: DM
Maternal-fetal: polyhydramnios, oligohydramnios, multiple gestation.
Fetal: abnormal karyotype, IUGR, macrosomia, fetal anomaly, abnormal lie.



- Infant weight < 10
th
percentile for a particular gestational age.
- Weight not associated with any constitutional or familial cause.

Incidence:
4-8 % of fetuses are diagnosed with IUGR



- FETAL causes:
Genetic causes:
Fetal chromosomal anomalies ( 2-5%) including: trisomies (18, 13, 21) & sex
chromosome abnormalities (decrease birth weight by ~ 15% but rarely account for
IUGR alone). Most chromosomally abnormal IUGR fetuses have associated structural
abnormalies, but 2% do not.
Single gene defects (3-10%) such as phenylketonuria, dwarsm.
Confined placental mosaicism (rare).

Fetal structural anomalies:
Cardiovascular anomalies.
Bilateral renal agenesis.
? single umbilical artery.

Multi-fetal gestation:
Risk of IUGR increases with fetal number.
Affects dizygous & monozygous twin pregnancies.
Worse in poly/oligo sequence (twin-twin transfusion syndrome).

- UTEROPLACENTAL causes:
Utero-placental insufficiency (25-30%)
Chronic hypertension, pre-eclampsia
Anphospholipid anbody syndrome (25% of chromosomally & structurally normal
IUGR fetuses have LAC or ACA posive mothers. If ACA posive hypertensive, > 50%
risk of IUGR).
Unexplained chronic proteinuria (23% risk of IUGR).
Chronic placenta abruption.

Velamentous insertion of umbilical cord.

- MATERNAL causes:
Drugs &/or toxin exposure:
Cigarette smoking: it decreases uteroplacental blood flow; risk of SGA infant is
increased tree fold over nonsmokers.
Alcohol: may cause dysmorphic features & IUGR (fetal alcohol syndrome).
Illicit drugs (cocaine, heroin): cause vasospasm & decreased uteroplacental blood flow,
(30% of pregnant women using cocaine will have SGA infant).

Malnutrition (especially gestational malnutrition superimposed on poor pregnancy nutritional
status)

Maternal medical conditions:
Hyperthyroidism, SLE, Diabetes mellitus, renal disease, Hemoglobinopathy (affects
maternal oxygenation so affects fetal growth), Chronic pulmonary disease, Cyanotic
heart disease, anemia, previous IUGR.

Infections:
Malaria (the single greatest cause of IUGR worldwide).
Rubella.
Cytomegalovirus
Toxoplasmosis
syphilis
? HIV
? Varicella




Compromise in uteroplaccental blood flow


Decreased nutrients (glucose, oxygen, amino acid, ? growth factors) to fetus


Fetal growth begin to diminish in a fixed sequence (sub-cutaneous tissue axial skeleton vital
organs such as brain, heart, liver, kidney)


Nutrients, oxygen & energy demands of the growing fetoplacental unit begin to exceed supply
leading to hypoxia, acidosis & death


Changing in antepartum fetal testing reflect the pathophysiology changes (in sequence):
1) Umbilical systolic/diastolic ratio increases as placental vascular resistance increases.
2) Fetal growth on U/S slow or stops.
3) Oligohydramnios develops due to diminish perfusion of the fetal kidneys.
4) Loss of fetal heart rate variability decelerations.
5) Fetus dies.




Q: how dose congenital infection affect fetal growth?
A: by interfering with cellular development; generally, the earlier the infant
infected, the more sever the outcome.




Symmetric/ type 1 (20%):
Occur early in pregnancy.
Inadequate growth of head & body.
Head abdomen ratio may be normal.
Usually associated with congenital anomalies or TORCH infections.

Asymmetric / type 2 (80%):
Occur late in pregnancy.
Brain is spared, therefore head abdomen ratio increased.
Usually associated with placental insufficiency.
More favorable prognosis than type 1.



Suspect the diagnosis in mothers at high risk.
Maternal fundal hight is considered as a screening test for diagnosis of IUGR.
If mother at high risk or the fundal hight lag was grater than 3-4 weeks, pelvic U/S & Doppler analysis of
umbilical cord are needed.

U/S should include assessment of:
Head circumference relative to abdominal circumference:
Establish head circumference to abdominal circumference ratios:
In normal fetuses: Before 32 weeks: HC/AC > 1.0
32 to 34 weeks: HC/AC = 1.0
Aer 34 weeks: HC/AC < 1.0
In fetus with asymmetric IUGR:
The head remains large relative to the body; therefore, HC/AC is elevated.
In fetus with symmetric IUGR:
Both HC & AC are reduced; the ratio remains normal.
Femur length (FL):
Used when fetal position prevent accurate measurement
Femur length spared in symmetric IUGR increasing FL/AC ratio
Amniotic fluid volume (AFV):
Decreased AVF may be an early sign of IUGR.
70% - 80% of IUGR fetuses are affected by oligohydramnios.





Placenta grade:


o Grade 0: NO calcifications & NO indentations in the chorionic plate.
o Grade 1: Few calcifications throughout the placenta.
o Grade 2: Calcifications along the uterine wall & indentations in the chorionic
plate.
o Grade 3: significant calcium deposits & indentations in the chorionic plate
that appears to outline individual cotyledons.

Q: what is the fundal hight lag?
A: a fundal hight smaller than fetal gestational age.
Q: Why dose decreased AFV occurred in IUGR?
A: Decreased renal blood flow secondary to shunting to other organs
lead to decreased fetal urine output & thus decreased AFV.


Q: what indices are evaluated in placental grading?
A: placental calcium deposited & indentations in the chorionic plate.

A placenta of higher grade than expected for a gestational age may indicate
decreased in placental function & subsequent IUGR.

Estimated fetal weight:
Established charts & formulas determine EFW using biparietal diameter (BPD), HC, AC &
FL.
Fetal gestational age: a MUST prior to assessing for IUGR; do not confuse a misdate fetus with a
fetus with symmetric IUGR.
Congenital anomalies: may indicate a chromosomal anomalies.



Doppler flow studies:
It can be used to evaluate uterine umbilical or fetal middle cerebral artery blood flow.
Normally there will be a Forward flow through the umbilical arteries throughout the cardiac cycle.
Decreased end diastolic ow with a corresponding increased systolic/diastolic rao (S/D rao > 2.6)
may indicate IUGR. Most reliable no diastolic flow.



- Risk modification prior to pregnancy.
- Modify controllable factors: smoking, alcohol, nutrition & treat maternal illness.
- Bed rest.



General goal of monitoring fetus with suspected IUGR:
To balance the risk of delivering a premature infant against the risk of stillbirth.

Principles of management including:
Identification of women at high risk.
Early antepartum diagnosis.
Determination of etiology.
Regular fetal testing.
Appropriate timing of delivery.

Management plan for fetus with IUGR:
Attempt to determine etiology (U/S for fetal anomalies, check karyotype, exclude infectious
etiology).
Serial examination of the fetus.
Maternal education about daily fetal activity (kick counts).
Serial U/S examinaon every 3-4 weeks to evaluate the HC/AC rao, EFW, possible congenital
anomalies, AFV.
Regular fetal monitoring: frequent non-stress tests (NST) contraction stress test (CST), biophysical
profile (BPP) or Doppler studies if a fetus has nonreactive NST (especially if the fetus had a previously
reacve NST); CST posive (fetal heart rate deceleraons in > 50% of contracons) in 40% of IUGR
fetuses.
Possibly amniocentesis to time the delivery of the fetus.
Consider delivery when once a favorable gestational age is reached (34 weeks), once fetal lung
maturity is documented (either an L/S rao > 2 or the presence of phosphadylglycerol on
amniocentesis), or for worsening fetal testing (deterioration in biophysical profile, development of
oligohydramnios, the development of reversed end-diastolic flow on umbilical Doppler). I that

Q: What are the most useful U/S criteria for determining IUGR?
A: EFW below 10
th
percentile, decreased AFW, elevated HC/AC.
case steroid is given to accelerate lung maturity with close fetal monitoring if the amniocentesis
indicate fetal lung immaturity.
Intrapartum management continuous fetal heart rate (FHR) monitoring:
If reassuring FHR normal delivery
If persistent FHR decelerations possible C/S.
After delivery send placenta/fetal membrane to pathology to look for evidence of vasculopathy.



- Greater risk of perinatal mortality & morbidity.
- Prone to meconium aspiration, asphyxia, polycythemia (secondary to fetal hypoxia & an increased
production of RBCs to compensate for the decreased oxygenation), hypoglycemia, pulmonary
hemorrhage & cerebral dysfunction (ranging from minor learning difficulty to cerebral palsy),
hypothermia (due to decreased body fat stores).
- Common metabolic derangements in IUGR infants: Hypoglycemia, Hypokalemia, Hyponatremia,
Hyperphosphatemia

Q: What are the etiological factors of hypoglycemia?
A: 1) decreased glycogen stores secondary to malnutrition.
2) decreased sensivity of gluconegenesis pathway to hypoglycemia.

Normal Labor & Dystocia
Prepared by: Mohammad Bokhary - 6
th
year student - 2008
Sources: OB Recall Toronto Notes 2007 Baby pink sheets Clinical sessions



Its a Regular uterine contractions, causing progressive effacement & dilatation of the cervix, leading to
expulsion of the fetus & placenta.
Regular uterine contractions : at least 2 contracons in 10 min.
Cervical effacement: SHORTENING of cervix & thinning of the walls. Measured in percent %
Cervical Dilatation: cervix is stretching beyond normal DIMENTIONS. Measured in CM.










Definitions you should know:
Fetal Lie : relation of fetal long axes to maternal long axes (longitudinal, transverse).
Fetal Presentation : which part of fetus arriving first in the birth canal :
o Cephalic: vertex, face.
o Breech: complete, incomplete, frank -refer to abnormal position & presentation-.
o transverse.
Fetal Position : which anatomic part of fetus is related to maternal symphysis pubis :
o OA (Occiputo-anterior) Left OA is the most common position
o OP (Occiputo-posterior) mostly rotates spontaneously during labor.
o How to determine the position? By sutures of fetal skull.
Fetal Station: relation of fetal BONY presenting part to ischial spines.
o 0 : fetus is engaged
o -1 to -5 CM above ischial spines
o +1 to +5 CM below ischial spines
Engagement: decent of fetal BIPARAITAL (if cephalic) or INTERTROCHANTRIC (if breach) diameter
through the pelvic inlet.
Crowning : the largest diameter of fetal presenng part in encircled by VULVAR ring. (staon +5)
False labor (Braxton hicks contractions):
Not regular, Not associated with effacement or
dilatation

What is TERM? Delivery of the fetus within 40w 2 weeks
What is POST-TERM? Delivery of the fetus aer 42 weeks
What is POST-DATE? Pregnancy has passed the EDD (weather term or post-term)




1. 1
st
Stage :
starting from the onset of contractions, til full CERVICAL effacement & dilatation.
o Duration: (Primigravida : up to 18 h), (mulgravida: up to 10 h).
o Latent phase : Irregular contractions, effacement , slow dilatation (up to 4 cm).
o Active phase : Regular contractions, full effacement full dilatation.
Dilatation rate : (Primigravida : 1.2 cm/h), (mulgravida: 1.5 cm/h).
Maximum slope in Friedman curve- to be discussed in dystocia-

2. 2
nd
Stage :
starting from full CERVICAL effacement & dilatation, till expulsion of FETUS.
o Duration: (Primigravida : up to 2 h, 3 with epidural analgesia), (mulgravida: up to 30
min).
o Cardinal movements: Engagement Decent Flexion Internal rotation extension
external rotation.

3. 3
rd
Stage :
starting from expulsion of FETUS, till expulsion of PLACENTA.
o Duraon: no more than 30 min (prime/mul)

4. 4
th
stage:
rst 1 hour post partum.



Always remember :
1. History
2. Examination
3. Investigations to order :
Blood profile (CBC, Group, cross match)
Serology screen -if not booked- (HIV, HBV, Syphlis VRDL)

1
st
stage (cervical dilatation & descent):

Maternal Care Fetal Care

Any comfortable position, common is lateral
recombent

Orders :
NPO
IV fluids (ringer lactate)
Empty bladder
Fecal enema NaPO
4

Shave & clean Pubic and vulvar area
Insert IUPC (intra uterine pressure
catheter)
if ROM (rupture of membranes) occur

Vaginal Examination every 2 hours to check :
Cervix (Bishop score) -see induction of
labor-
Membrane : intact/rupture
Fetal head molding
Pelvic adequacy

Analgesia :
Systemic
o Pethidin 50-100 mg / 2-3 hours
o IV /IM
Regional
o Epidural / Spinal
Inhalation
o N
2
O (50% Nitrox oxide + 50%
O
2
)


Monitor fetal Heart
Every 30 min
Every 15 min if high risk

How to monitor ?
CTG most important
Doppler with each contraction
Feto-scope

Amniotomy if the method of Inducon / Augmentaon during stage 1


2nd stage (Delivery of fetus):

Maternal Care Fetal Care

Lithotomy position. Increases lumbosacral
diameter

With each contraction, tell mother to bear
down. Rest between contractions.

Episiotomy :
Surgical incision in perineum
Preformed when the presenting part
separates the 2 labia apart by 4 cm or
more.
It is done to:
o Increase vulvar outlet
diameter
o Prevent lacerations & tearing
(read below)
o Prevent relaxation of pelvic
floor
Indications
o Primigravida
o Breech presentation
o Shoulder Dystocia
o Instumental delivery
Types
o Midline
o Mediolateral
o J-shaped

Lacerations Grades:
1
st
grade : vaginal mucosa / skin
2
nd
grade : vaginal wall / perineal
muscles
3
rd
grade : reached Anal sphincter
4
th
grade : involved rectal mucosa


Monitor fetal Heart
Every 15 min
Every 5 min if high risk

Ritgens maneuver
Hand behind rectum making UPWARD
pressure
Hand over fetal occipit making
DOWNWARD pressure
Used to guide the expulsion prossess.

Suction of OroNasoPharinx
Prevent aspiration
Prevent vagal response -> bradycardia
Used to guide the expulsion prossess.

Deliver shoulders
Anterior : do gentle downward traction
Posterior : elevated head upward

Cord
Nucule ? ( )
o Loose ? slide it off
o Tight ? clamp then cut
How to cut ?
o Hold by 2 metallic clamps 4 cm
away
from each other.
o Cut between
o Replace babys clamp by plasc 2
cm away from abdomen.
o Cut within 30 sec.
Earlier = anemia
Later = jaundice




3
rd
stage (Expulsion of PLACENTA):

Maternal Care Placental Care

When anterior shoulder is delivered (During
stage 2):
Oxytocin 5 units IM

When baby is delivered (End stage 2):
Methergene 0.2 gm IM

Delivery of placenta ----------------------------------
----->

After placenta delivery :
Fundal massage
Oxytocin 20 units IV

Do CCT (Controlled Cord Traction)
1 hand HOLDING the cord (not tracon)
1 hand PUSHING the fundus upward toward
umbilicus
By continuous pushing, placenta will be
separated

Sings of placental separation
Elongation of the cord
Gush of blood
Rise of the fundus

Was the placenta completely expelled ?
Yes ? go stage to 4
No, incomplete
o No bleeding ? wait up to 1 hour
o Bleeding ? do manual removal
under general anesthesia.


4
th
stage (rt 1 hour post-partum):

Monitor:
Vitals
Uterine involution : should be at level of umbilicus
o If above uterus, what do you call it ? Sub-involuted uterus (causes are same of uterine
atony)
Lochia
Repair lacerations

Examine cord for:
Missing vessel (30%)
o associated with anomalies
o mainly RENAL anomalies
extra vessel (1%)

Take fetal blood sample :
Fetal HB & blood group

Induction & Augmentation of Labour
Prepared by: Wafaa Al-Ahmadi.
Source: Toronto Notes 2008 + Obstetrics & gynecology At Glance + Tarek Arab sheet.




Artificial initiation of labour before its spontaneous onset for the purpose of delivery of the fetus &
placenta.




Absolute indications Relative indications
Maternal indications:
Preeclampsia/eclampsia
Maternal medical problems (DM, chronic
renal failure, chronic pulmonary disease)
Maternal indications:
Chronic HTN
Pregnancy induced HTN
Gestational diabetes
Logistic factors
Risk of rapid labour
Distance from the hospital
Psychosocial indications
Fetal indications:
Chorioamnionitis
Abnormal antepartum testing
IUGR
Post-term pregnancy (>42 weeks)
isoimmunization
Fetal indications
PROM
Fetal macrosomia
Fetal demise
Previous stillbirth
Fetus with a major congenital anomalies
Utero-placental indications:
placenta abruption
Utero-placental indications:
unexplained oligohydramnios




Absolute contraindications Relative contraindications
Maternal contraindications:
Active genital herpes
Serious chronic medical conditions &
unstable maternal conditions
Maternal contraindications:
Cervical carcinoma
Pelvic deformities
Fetal contraindications:
Mal-presentation
Fetal distress
Premature fetus without lung maturity
Fetal contraindications:
Extreme macrosomia
gross cephalo-pelvic disproportion
Utero-placental contraindications:
Placenta previa
Vasa previa
Prior classical C/S

Utero-placental contraindications:
Low-lying placenta
Unexplained vaginal bleeding
Cord presentation
Myomectomy involving the uterine cavity



Induction of labour is indicated when the
risk of continuing pregnancy exceeds the
risk associated with induced labour &
delivery.




Confirm indication of induction.
Confirm gestational age.
Patients consent.
Capability for C/S if necessary.
Maternal:
- Short, thin, soft anterior cervix with open os (inducible or ripe)
- If cervix is not ripe, use prostaglandin (cervidilTM or prepidilTM)
Fetal:
- Reassuring fetal heart tracing.
- Cephalic presentation.
- Adequate fetal monitoring available.
- Assessment of fetal lung maturity

Q: how to assess fetal lung maturity?
A: amniocentesis is necessary unless one of the following is met:
1) Documented fetal heart tones for 20 weeks by fetoscope/30 weeks by Doppler.
2) Posive serum/urinary pregnancy test at least 36 weeks prior.
3) U/S between 6-11 weeks that support gestaon of 39 weeks or more.
4) U/S obtained between 12-20 weeks that conrms a gestaonal age of 39 weeks
determined by clinical history & examination.


Likelihood of success determined by Bishop score: (see the table below)
Cervix considered unfavorable if < 6
Cervix favorable if > 6
Score of 9-13 associated with high likelihood of vaginal delivery

Cervical
characteristic
0 1 2 3
Position Posterior Mild anterior -
Consistency Firm Anterior Soft -
Effacement (%) 0.30 40-50 60-70 >80
Dilatation (cm) 0 1-2 3-4 5
Station of fetal
head
-3 -2 -1 or 0 +1




Failure to achieve labour &/or vaginal birth.
Uterine hyper-stimulation & fetal compromise.
Uterine rupture.
Uterine atony & PPH.
Maternal side effects to medications.





Consider the following before
induction:
Indication for induction
Contraindications
GA
Cervical favorability
Fetal presentation
Potential for CPD
Fetal well-being/FHR
Membrane status




CERVICAL RIPENING:

Definition:
Use of medications or other means to soften, efface & dilate cervix to increase likelihood of induction
success.
Ripening of an unfavorable cervix (Bishop score < 6) is warranted prior to inducon of labour.

Methods:
Intra-vaginal prostaglandin PGE2 gel (Prostin gel): long & closed cervix with no ROM.
- Recommended dosing interval of prostaglandin gel is every 6 to 12 hours up to 3 doses.
Intra-vaginal PGE2 (CervidilTM): long & closed cervix, may use if ROM, continuous release,
can be removed if needed.
- Controlled release PGE2
Misoprostol: synthetic methylated PGE1 (not commonly used).
Foley catheter placement to mechanically dilate the cervix.
Hydroscope dilators, osmotic dilators (laminaria).









Amniotomy:
Artificial rupture of membranes (amniotomy) to stimulate PG synthesis & secretion; may try
this as initial measure if the cervix is dilated.
Few studied address the value of amniotomy alone for induction of labour.
Amniotomy + IV oxytocin: more women delivered vaginally at 24 hours than amniotomy alone
(relave risk = 0.3) & had fewer instrumental vaginal deliveries (relave risk = 5.5).

Oxytocin:
Oxytocin (pitocin
TM
): 10 U in 1L NS run at 0.5-2 mU/min IV increasing by 1-2 mU/min
q20-60 min to max. of 36-48 mU/min.
Oxytocin alone reduced rate of unsuccessful vaginal deliveries within 24 hours (8.3% vs 54%,
RR 0.16%). The ideal dosing regime of oxytocin is not known. It is currently recommended to
use the minimum dose to achieve active labour with an increase every 30 minutes or more.
Reassessment should occur once a dose of 20 mU/min is reached.
Complications of oxytocin:
- Hyperstimulation/titanic contraction (may cause fetal distress or rupture of uterus).
- Uterine muscle fatigue, uterine atony (may result in PPH).
- Vasopressin-like action causing anti-diuresis.
- Water intoxicaon with convulsions & coma when infused for more than 24
hours (though rare).
- Cord prolapsed.
- Placental abruption.


- Intra-vaginal prostaglandins are associated with higher rate of uterine
hypertonus, uterine hyperstimulatin, & fetal heart rate abnormalities.
- Prostaglandins are associated with reduced rate of C/S, instrumental
vaginal delivery & failed induction.
Oxytocin t
1/2
= 3.5 min



It is used to promote adequate contractions when spontaneous contractions are inadequate &
cervical dilatation or descent of the fetus fails to occur (in the absence of absolute cephalo-pelvic
disproportion).

Method:
Include amniotomy and/or oxytocin (0.5-2 mU/min IV increasing by 1-2 mU/min q20-60
min to max. of 36-48 mU/min).
Abnormal Labor & Delivery
Prepared by: Wafaa Al-Ahmadi
Source: Toronto Notes 2008 + Obstetrics & Gynecology At Glace + Obstetrics & Gynecology Recall


Labor Dystocia


- Expected patterns of descent of the presenting part & cervical dilatation fail to occur in the appropriate
time frame; can occur in all stages of labor (see figure below).
- During acve phase: > 4hrs of < 0.5 cm/hr.
- During second phase: > 1 hr with no descent during acve pushing.



(the 4 Ps of dystocia: Power, Passenger, Passage, Psyche)
Power (leading cause): contractions (hypotonic, incoordinate), inadequate maternal expulsive
efforts.
Passenger: fetal position, attitude, size, anomalies (hydrocephalus).
Passage: pelvic structure (cephalo-pelvic disproportion), maternal soft tissue factors (tumors, full
bladder or rectum, vaginal septum).
Psyche: hormones released in response to stress can bring about dystocia.
- Psychological & physiological stress should be evaluated as part of management once
dystocia has been diagnosed.















Arrest Disorder (curve C):
Arrest dilatation
- Dilatation progress does not occur for 2 hrs in a paent who has entered the acve phase.
- Arrest usually occur at a cervical dilataon of 5-8 cm.

Arrest of descent
- No progress in staon for >1 hr during second stage.
- Should search for factors causing CPD (nearly 50%; require C/S).
- CPD diagnosed if adequate contraction measured by intrauterine pressure catheter (IUPC) with no
descent/dilataon for > 2 hrs.
- If CPD ruled out, IV oxytocin & amniotomy can be attempted.

Protraction disorders (curve D):
Protracon of dilataon: slope of cervical dilataon is < 1.2 cm/hr in primigravidas or < 1.5 cm/hr
in multigravidas.
Protracon of descent: a rate of descent of < 1.0 cm/hr in primigravidas or 2.0 cm/hr in
multigravidas.
Treatment: oxytocin augmentation if contractions are inadequate amniotomy.

Prolonged latent phase (curve E):
20 hrs in primigravidas or 14 hrs in mulgravidas during which labor has not progressed to the
active phase.
Most often due to false labor (avoid amniotomy for fear of false labor & increased risk of
intrauterine infection).
Premature or excessive use of sedation or analgesia may play a role.
Careful search for factors of CPD should be made.
Management: oxytocin augmentation if diagnosis of labor is certain, otherwise rest sedation.

Risks of dystocia:
Inadequate progression of labor is associated with an increase incidence of:
-Maternal stress.
-Maternal infection.
-Postpartum hemorrhage.
-Needs for neonatal resuscitation.






























Malpresentation

Definition:
Fetus presenting buttocks first (position of breech is defined
relative to the sacrum).
Diagnosis:
By leopoids maneuver, vaginal exam or U/S.
Incidence: 3-4% of term deliveries.

Risk factors:
Prematurity (28% breech at 28 weeks, 15% at 30 weeks).
Uterine anomalies.
Polyhydramnios.
Previous breech delivery.
Multiple gestation.
Placenta previa.
Fetal anomaly (anencephaly, hydrocephalus).

Associated with:
2 fold increased risk of congenital abnormality
Increased risk of cord prolapse.
Preterm labor, birth trauma, ,maternal morbidity.

Types of breech:
Frank breech (70%).
Complete breech (10%).
Footling or incomplete breech (20%).

External cephalic version (ECV):
Definition:
Refers to attempted conversion of breech to vertex presentation by manual manipulation
through the maternal abdomen.
Performed aer 36 weeks.
Benefits: decrease the incidence of breech at term.
Risks of ECV:
-Fetal disress.
-Abruption.
-Cord accident.
-Rupture of fetal membranes.
-Neurological injury.
Contraindications to ECV:
Absolute contraindication uterine anomaly
Relative contraindications prior C/S, IUGR, twins, oligohydramnios, labor.

Predictors of success:
Frank breech.
Normal amniotic fluid volume.
Operator experience.
Non-engaged breech.
Multiparous & thin mother.
Laterally located fetal spine.

Techniques of ECV:
36 weeks, no labor, RhoGAM consent obtained, NST, RhoGAM if needed.
Under U/S guidance.
epidural/beta mimetic tocolytsis.
Check NST after ECV.

Success rate: 50-70%

Vaginal breech delivery:
Preterm singleton breeches are best delivered by C/S (because of risk of head
entrapment).
Term breech fetuses are most commonly delivered abdominally (because if the high risk
of head entrapment, cord prolapse, asphyxia, birth trauma with vaginal breech delivery).
Vaginal breech delivery is a safe alternative to C/S under the following conditions:
Term frank breech.
Esmated fetal weight 2500-4000g by U/S.
No hyperextension of fetal head.
Adequate pelvimetry (clinical, X-ray or CT pelvimetry).
Capacity for emergency C/S.
Experienced operator.
Adequate anesthesia.
Adequate progress in labor.
Absence of fetal distress.
Preferably multiparous women proven pelvis




Incidence: 0.3% of term pregnancies.
Etiology:
-Prematurity.
-Placenta previa.
-Grandmultiparity.
-Multiple gestation.
-Uterine anomalies (fibroid, bicornuate uterus).
Management: conceder ECV, C/S if unsuccessful.



- Malpresentation can occur in vertex fetus. Some can be delivered vaginally (such as occiput
posterior, face with mentum {chin} anterior). In others (brow, face with mentum posterior),
conversion to occiput anterior is necessary for vaginal delivery.

- Compound presentaon (<0.1% of all deliveries) refers to the presence of a fetal extremity
alongside the presenting part, it is associated with prematurity, polyhydramnios, & multiple
gestation. Vaginal delivery can often be effected.

- Funic presentation: refers to presentation of the umbilical cord below the head. It is rare. If
identified in labor, C/S may be indicated because of the risk of cord prolapse.



Intrapartum complications


Definition:
Impaction of the anterior shoulder of the fetus against symphysis pubis after fetal head
has been delivered.
Life threatening emergency.

Etiology/Epidemiology:
Incidence 0.15-1.4% of deliveries.
Occurs when breadth of shoulders is greater than biparietal diameter of the head.

Risk factors:
Maternal: obesity, diabetes, multiparity.
Fetal: prolonged gestation, macrosomia.
Labor: prolonged 2nd stage, prolonged deceleraon phase (8-10 cm), instrumental mid-
pelvic delivery.

Clinical features:
Turtle sign (head delivered but retracts against inferior portion of pubic symphysis).
Complications:
Chest compression by vagina or cord compression by pelvis can lead to hypoxia.
Danger of brachial plexus injury (Erb palsy: C5-C7; Klumpkes palsy: C8-T1) 90% resolved
within 6 months.
Fetal fractures (clavicle, humerus, cervical spine).
Maternal perineal injury, may result in PPH.
Intrapartum fetal hypoxia or trauma.

Treatment:
Goal: to displace anterior shoulder from behind symphysis pubis; follow a stepwise approach of
maneuvers until goal achieved (see box)
Approach to the management of shoulder dystocia: ALARMER

Apply suprapubic pressure & ask for help.
Legs in full flexion (MecRoberts maneuver).
Anterior shoulder disimpaction (suprapubic pressure).
Release posterior shoulder.
Manual corkscrew.
Episiotomy.
Rollover (on hands & knee).

Other options:
-Cleidoctomy (delibration fracture of neonatal clavicle).
-Zavanelli maneuver: replacement of fetus into uterine cavity & emergent C/S.
-Symphysiotomy.
-Abdominal incision & shoulder disimpaction via hysterectomy subsequent vaginal delivery.

Prognosis:
90% of shoulder dystocia will resolve with McRoberts maneuver & suprapubic pressure.
1% risk of long term disability for infant.




Definition: An obstetric emergency characterized by prolapse of the umbilical cord into the vagina
after rupture of the fetal membranes.

Incidence: 0.4% of term cephalic pregnancies.

Risk factors:
Malpresentation (breech, transfers lie).
Polyhydramnios.
Small fetus.
Prematurity.

Diagnosis: Palpation of pulsatile cord on vaginal examination with or without fetal bradycardia.

Prevention: Perform amniotomy only once the vertex is well applied to the cervix, & always with
fundal pressure.

Management: replace cord manually & expedite delivery immediately (usually by emergency C/S).



Facial nerve paralysis:
Result from pressure on the facial nerve.
It is more common after operative vaginal (forceps) delivery.
Resolution is usually complete within few days.

Injuries to the neck & spinal cord:
Result from excessive traction at delivery with fracture or dislocation of the vertebrae.
Such injuries may prove fatal.

Multicystic encephalomalacia.




Incidence: 4-5% of term infants will have sonographic evidence of IVH unrelated to obstetric factors.
Risk factors:
Prematurity.
Fetal bleeding diathesis.
Alloimmune.
Thrombocytopenia.
Birth trauma is an uncommon cause of intracranial hemorrhage.

Treatment: primarily supportive. Surgery is rarely indicated.
Preterm Labour (PTL)

Prepared by: Roa'a mursi
Sources: Obstetrics & Gynecology Recall + Toronto Notes 2008+ Obstetrics & Gynecology at Glance +
obstetric illustrated+ Hacker



Contraction and progressive cervical change between 20 and 37 completed weeks of gestation.)








7-10% of all deliveries.
Accounts for 50%-70% of all neonatal deaths not caused by congenital anomalies.
All preterm births caused by preterm labor is 30% approximately.



Idiopathic:
Called: (intact membrane) OR (spontaneous preterm birth)
(Most common)

Maternal cause:

General:
1. Maternal age: < 18 or > 40
2. Hx of preterm births(17%-37% risk aer one preterm births)
3. Low preganacy weight.
4. Repeated second trimester spontenous abortion.
5. Nonwhite race
6. socio-environmental (poor nutrion, smoking > 10 cigarees\ days , drugs, alcohol, stress, lack of
prenatal care)
7. infection :
(recurrent pyelonephritis, untreated bacteriuria, chorioamnionitis)
genital infection (bacterial vaginosis (BV) is associated with a two fold increase in relative risk of
preterm birth)
ex: group B streptococcus (GBS), gonorrhea, Chlamydia, Ureaplasma, syphilis, trichomoniasis,
gardnerella
8. HTN, DM, chronic illness
9. mechanical factors, previous obstetric, gynecological and abdominal surgeries

Local:(uterine and cervical cause)
Congenital: septate, unicornuate or bicornuate
Traumatic: incompetent cervix,, excessive enlargement (hydramnios), use of IUD.

Inflammatory: ashermans
Cervical incompetence is premature cervical dilation but
in the absence of contraction before term..

Neoplastic: leiomyomas

Maternal-fetal:

1. Placental anomalies.
2. PPROM (30-35% of all preterm birth)
3. Polyhydramnios
4. Placenta previa
5. Abruption, placental insufficiency.

Fetal:

1. Mulple gestaon( 10 % of all preterm)
2. Congenital abnormalities of fetus
3. Fetal hydrops
4. Fetal death.
5. Isoimmunisation.




Between 20 weeks and 37 weeks is based on the following criteria in the paents with ruptured or intact
membranes:
Regular uterine contracons (2 in 10 minutes or 4 in 20 minute OR 8 in 60 minute)
Documented change in cervix (cervix >2 cm dilated or 80% eaced.)

















Conditions should be ruled out in preterm labor:

1. PPROM
2. Placental abruption
3. Placenta previa
4. Fetal death
5. Infection
6. Multiple gestation
7. Fetal anomalies

What questions should be asked in the history of preterm labor patient?
Does the patient have:
1. A Hx of preterm birth?
2. A Hx of cystitis or pyelonephritis?
3. A known multiple gestation?
4. A known placenta previa?
5. A known fetal anomaly?
6. A known uterine anomaly?
7. Good fetal Movement?
8. Untreated infection?
9. Cigarette or cocaine use?
10. accurate LMP or dating US.?






A. Initial (bed rest & hydration)

Transfer to appropriate facility if stable
Hydration (NS @ 150 mLlhour)
Bed rest in LLDP (lateral decubitus position)
Sedation (morphine)
Avoid repeated pelvic exams (increased infection risk)
V/S examination of fetus (for GA, BPP, position, placenta location, estimated fetal
weight (EFW)
Prophylactic antibiotics; controversial but may help delay delivery,
important to consider if PPROM

B. Suppression of Labour Tocolysis

Does not inhibit preterm labour completely, but may buy time to allow Celestone use/transfer
to appropriate centre.
Requirements - all must be satisfied
preterm labour
Live, immature fetus, intact membranes, cervical dilatation of <\= 4 cm
Absence of maternal or fetal contraindications.


Contraindications:
Maternal:
Bleeding (placenta previa or abruption), maternal disease (hypertension,
diabetes, heart disease), pre-eclampsia or eclampsia, chorioamnionitis.

Fetal:
Erythroblastosis fetalis, severe congenital anomalies, fetal
distress/demise, ruCR, multiple gestation (relative)


Tocolytic procedure
Ensure availability of necessary personnel and equipment to assess mother
andfetus during labour and care for baby of the predicted CA if therapy fails
If no contraindications present, agent used depends on clinical situation
Proven efficacy
Calcium channel blockers: nifedipine
Prostaglandin (PC) synthesis inhibitors (2nd line agent): indomethacin
Beta-mimetics: ritodrine, terbutaline (rarely used)
Should be used only for: 8 hrs, and/or transfer to an appropriate facility.
No proven efficacy
nitroglycerin patch: vasodilator and smooth muscle relaxant that may delay
delivery by 24-48h
magnesium sulfate (if diabetes or cardiovascular disease present)











C. Enhancement of Fetal Pulmonary Maturity

Betamethasone valerate (Celestone) 12 mg 1M q24h x 2 or dexamethasone 6 mg 1M q12h x 4.
28-34 weeks CA: reduces incidence of respiratory distress syndrome (RDS)
24-28 weeks CA: reduces severity of RDS, overall mortality and rate of intraventricular
hemorrhage (IVH)
Specific maternal contraindications: active TB, viral keratosis, maternal DM


D. Cervical Cerclage

Definition:
Placement of a cervical sutures, wires or synthetic tape at the level of the internal os, usually at
the end of the first trimester and removed in the third trimester.

Indications:
Cervical incompetence (CI) - cervical dilation and effacement in the absence of increased uterine
contractility

Diagnosis of CI
Obstetrical Hx: silent cervical dilation
Ability of cervix to hold an inflated Foley catheter during a hysterosonogram.


Proven benefit in the prevention of PTL in women with primary structural abnormality of the
cervix (e.g. conization of the cervix, connective tissue disorders)

Benefit is variable in those with secondary cervical incompetence causing premature ripening of
the cervix (e.g. infection, abnormal placentation)



Complication & Prognosis:
Prematurity is the leading cause of perinatal morbidity and mortality
30 weeks or 1500 g (3.3lbs) = 90% survival
33 weeks or 2000 g (4.4lbs) =99% survival
Morbidity due to asphyxia (may lead to cerebral hemorrhage), hypoxia (may lead to
necrotizing enterocolitis), sepsis, respiratory distress syndrome (RDS), intraventricular
hemorrhage, thermal instability, retinopathy of prematurity, bronchopulmonary dysplasia




Short term tocolysis goal: prevent delivary for at least 48 hs to
allow administration of glucocorticoids to mother.

Long term tocolysis goal: allow fetus to gain lung maturity in
utero to increase the chance of a good outcome after delivary.


Prevention of Preterm Labour
Currently there are no agents approved by Health Canada to arrest preterm labour
Good prenatal care, identify pregnancies at risk, treat silent vaginal infection or UTI,
patient education.

Prevenon based on at least 3 potenal causal pathways:

Infection-cervical pathway Placental-vascular
pathway(PVP-1)
Stress-strain pathway
1. Treatment of bacterial
vaginosis has reduced
the incidence of
preterm delivary.

2. bacterial vaginosis
(Rx - metronidazole)
and ureaplasma
urealyticum
(Rx - erythromycin)

3. There is a link between
vaginal-cervical
infection & progressive
changes in cervical
length, as measured by
vaginal
ultrasonography.

4. The relative risk of
preterm birth increase
from 2.4 for cervical
length (3.5cm) to 6.2
for a length of (2.5 cm)

5. Other recent test:
Cervical & vaginal fetal
fibronectin.
This substance is a glycoprotein
produced by fetal membranes.
Functioning to maintain
integrity of chorionic-
decidual interface.
Positive (>50 ng/mL) at 22
to 24 weeks predicts more
than 1\2 of SPL that occur
before 28 weeks.
DDx of +ve fibronectin:
Short cervix
Vaginal infection
Uterine activity
Begins early at time of
implantation when there are
important changes taking
place at the placental\
decidual \ myometrial
Interface.

Alteration in normal early
changes are important role
in pathophysiology of poor
fetal growth, important
component of preterm birth,
fetal growth restriction and
preeclampsia.

The normal early changes
are:
1- important immunological
changes
(switch Th-1=embryotoxic to
Th-2=block Ab producon
that prevent rejection)
2- trophoblasts are invading
the spiral artries of the
deciduas and myometrium.
Cognitive & work releated
stress( as poor nutrition and
fasting) and strain


Increase cortisol&
catecholamine.



Cortisol:Initiate placental
corticotrophin-releasing H.
(CRH)
and catecholamine:
cause uterine contraction



Intiate labor at term.


**stress reduction & improved
nutrition are the only current
interventions.

Premature Rupture of Membranes


Prepared by: Roa'a Mursi
Sources: Obstetrics & Gynecology Recall + Toronto Notes 2008 + Hacker + obstetric illustradated



- premature ROM (PROM or amniorrhexis): spontaneous rupture of membranes prior to labour at
any GA
- prolonged ROM: >24 hours elapse between rupture of membranes and onset of labour.
- preterm premature ROM (PPROM): rupture of membranes before 37 weeks and prior to onset of
labour.
- Spontaneous rupture of membranes (SROM):spontaneous rupture of membranes AFTER onset
labour at any GA



Complicate 10% of all pregnancies
Associated with 30% of preterm births
94% of all cases occur at term.
5% occur in pregnancies with fetus weighng 1000-1500 g.
1% occur in fetus weighng < 1000g.











Maternal:
1. Multiparty
2. Infection (cervicitis, vaginitis, STD, UTI) most common
3. Over distention
- Fibroids
- Multipul G
- Hydramnios
4. Abruptio placentae
5. Cervical incompetence
6. Family history of PROM
7. Cerclage placement
8. Amniocentesis
9. Low socioeconomic class/poor nutrition, cigarette smoking




How does term and preterm pt. differ in their propensity to go into labor
after PROM?
Term pt:
90% in labor 24h aer PROM
Preterm pt. :
50% in labor 24h aer PROM.
75% in labor within 1 week aer PROM.

gush of fluid :
- Water-thick
- clear
- continuous : wrench cloths
- increase gush with cough
(valsalva manuver)
- no smell
(changes in these properties
could indicate infection)





















Fetal:
1. congenital anomaly
2. multiple gestation

Other risk factors
Associated with PTL



History:
Sudden gush of fluid from vagina followed by continuous leakage that may or may not be
associated with the passage of small amount of blood or mucus.

Examination:
General examination: nothing
Abdominal Examination: oligohydraminos.
Local examination: NO PV unless patient in labour
or inducon is decided amd the important 3 signs:
1. Pooling of vaginal fluid in the posterior fornix.
2. Positive nitrazine test-i.e : nitrazine paper reveals
PH > 6-6.5
(normal vaginal PH 4.5-6)
3. 'Ferning' on a slide prepared with thin layer of fluid obtained from the vaginal wall
& allowed to dry.








Organisms have been linked to PROM:
Ureaplasma urealyticum.
Trichomonas vaginalis.
Bacteroides species.
Chlamydia trachomatis
GP B streptococcus (GBS)
Gardnerella vaginalis and others.

How do they cause PROM?
By production of various factors may weaken fetal membranes and render them
susceptible to rupture.

Signs of infection:
- Fever - Tachycardia - Abdominal tenderness - fluid properties change
(color,smell,consistency)
- Leukocytosis - cultures +ve

: Ve culture + In
Unknown whether result of :
Infection causing PROM
through weakening of the
membranes. Or
PROM leading to
colonization with
microorganisms .
1. False positive nitrazine test occur if discharge is obtained from the cervical
OS because the cervical mucus like amniotic fluid, has a PH higher than
that of the vagina. Blood, semen, vaginitis can also raise PH.
2. Cervical mucus can also cause ferning.
3. Collect of fluid only from vaginal wall to avoid cervical mucus unless fluid
can be seen flowing from OS into the posterior fornix with valsalva
maneuvuver, cough, or fundal pressure.

















Preterm PROM:
The risk are primarily related to prematurity
(RDS, IVH, NEC)

Term PROM:
NO risk of prematurity, primary risk is infection




Visualization with sterile speculum (avoid introduction of infection)
pooling of fluid in the posterior fornix
May observe fluid leaking out of cervix on cough/Valsalva ("cascade")
Amniotic fluid turns nitrazine paper blue (low specificity as can be positive with blood, urine or
semen)
Ferning (high salt in amniotic fluid evaporates, looks like ferns under microscope)
Ultrasound to rule out fetal anomalies, assess GA and BPP, amniotic fluid volume for
oligohydrominos and fetal presentation.



Goal of the management:
- maximize fetal lung maturity
- deliver -regardless of GA- if signs of infection appears


General:
admit and monitor vitals q4h, daily BPP and WBC count
avoid introducing infection with examinations (do NOT do a bimanual exam)
cultures (cervix for GC, lower vagina for GBS)
assess fetal lung maturity by LIS ratio of amniotic fluid.

Prophylactic:
Aggressive treatment of vaginal infection during pregnancy.


Fetus\neonate mother
1. Neonatal sepsis
2. RDS
3. IVH( interventicular Hemorrhage)
4. PDA (patent ductus arteriosus)
5. NEC(necrotizing enterocolitis)
6. Pulmonary hypoplasia in fetus < 24
weeks.
7. Cord prolapse\intrauterine demise.
(complication of prematurity)

8. Chorioamnionitis
9. Endomyometritis
10. Puerperal sepsis





(complication of infection)
Active treatment:
Close observation for infection.
Antibiotic are given for variable periods according to duration of pregnancy.

< 24 weeks 26-34 weeks 34-36 weeks >36 weeks
(poor outlook
due to
pulmonary
hypoplasia)
The predominant
complication is
RDS
"grey zone"
where risk of
death from
RDS and
neonatal
sepsis is the
same.
the risk of death
from sepsis is
greater

Conservative
ttt
---------- -Corticosteroid
(predinsolone)
- Antibiotic.
--------- -----------
Active ttt
(termination
of pregnancy)
Treatment of
Choice.
Consider tocolysis
for 48h to permit
administration of
steroids if PPROM.
Indicated if:
- Infection is
developed.
- Maturity is reached
- Labour is started.
if the labour
dosen't start
with 48h
*ttt with
ampicillin
administration
induction of
labour..
but if the labour
dosen't start with
24h
*ttt with ampicillin
administration.

studies show broad spectrum coverage increases the time to onset of labour from PROM
by 5-7 days with no increase in maternal or neonatal morbidity or mortality
deliver urgently if evidence of fetal distress and/or chorioamnionitis





varies with gestational age
90% of women with PROM at 28-34 weeks GA go into spontaneous labour
within 1 week
50% of women with PROM at <26 weeks GA go into spontaneous labour
within 1 week


Postpartum Hemorrhage (PPH)
Prepared by: Wafaa Al-Ahmadi
Source: Obstetrics & gynecology At Glance + Toronto Notes 2008



Loss of > 500 ml of blood at the me of vaginal delivery, or > 1000 ml with C/S.
Incidence: 5-15%.



Early PPH:
- Define as PPH within the rst 24h aer delivery.
- Causes include: uterine atony, retained placenta fragments, lower genital tract lacerations,
uterine rupture, uterine inversion, abnormal placentation, coagulopathy.

Late or delayed PPH:
- Defined as PPH after 24h but within the rst 6 weeks.
- Causes include: retained placental fragments, infections (endometritis), coagulopathy, placental
site subinvolution.



- Previous Hx.
- Previous C/S.
- Coagulation defect.
- Retained placenta.
- Antepartum hemorrhage.
- Assisted delivery.
- Polyhydramnios & multiple gestation.
- Grand multiparity.
- Uterine malformation of fibroid.
- Prolonged & induced labor.



1- Uterine atony:
Most common cause of PPH
Avoid by giving oxytocin with delivery of the anterior shoulder.
Occur within first 24hs.
Risk factors: include uterine overdistension (due to polyhydramnios, multiple gestation,
fetal macrosomia), high parity, rapid or prolonged labor, infection, prior uterine atony, &
use of uterine relaxing agents (terbutaline, magnesium, anesthetics).

2-Pertained placental fragments:
Definition: Placenta undelivered aer 30 minutes ppostpartum.
Etiology:
May result from retenon of a cotyledon or succenturiate lobe (seen in 3% of placentae).
Examination of the placenta may indentify defects suggestive of retained products.
However, the majority of cases probably reflect abnormal placentation.
Risk factors: Placenta previa, previus C/S, post-pregnancy curettage, prior manual placenta
removal, uterine infection.
Investigation:
o Explore uterus.
o Assess degree of blood loss.
Management:
o 2 large bore IVs, type & screen,
o Brant maneuver (firm traction on umbilical cord with one hand applying suprapubic
pressure to hold uterus in place).
o Oxytocin 10 IU in 20 ml NS into umbilical vein.
o Manual removal if the above fails.
o D&C if required.

3-Lower genital tract lacerations:
Risk factors: include assisted vaginal delivery, fetal macrosomia, precipitous delivery, & use
of episiotomy.
Diagnosis should be considered when vaginal bleeding continues despite adequate uterine
tone.

4-Uterine rupture:
Incidence: 1 in 2000 deliveries.
Risk factors: include prior uterine surgery, obstructed labor, excessive use of oxytocin,
abnormal fetal lie, grandmultiparity, & uterine manipulations in labor (forceps delivery,
breech extraction, & intra-uterine pressure catheter insertion).

5-Uterine inversion:
Incidence: 1 in 2500 deliveries.
Definition: uterine prolapsed through cervix vaginal introitus.
Risk factors: include uterine atony, excessive use of tocolytics, excessive umbilical cord
traction, manual removal of placenta, abnormal placentation, uterine anomalies, & fundal
placentation. It is more common in grand multiparity.
Clinical features: can cause profound vasovagal response with vasodilation & hypovolemic
shock. Shock may disproportionate to maternal blood loss.
Management:
o Urgent management essential, call anesthesia.
o ABCs initiate IV crystalloids.
o Can use tocolytic drug (e.g. terbutaline) or nitroglycerin IV to relax uterus & aid
replacement.
o Replace uterus without removing placenta.
o Remove placenta manually & withdraw slowly.
o IV oxytocin infusion (only after uterus replaced).
o Re-explore uterus.
o May require GA laprotomy.

6-Abnormal placentation:
Includes:
o Abnormal attachement of placental villi to the myometrium (acreta).
o Inavasion into the myometrium (increta).
o Penetration through myometrium (percreta).


Risk factors: prior uterine surgery, placenta previa, smoking, & grand multiparity.
Placenta acreta is the most common type
of abnormal placentation occurring in
around 1 in 2500 deliveries.

7-Coagulopathy:
Congenital coagulopathy: complicate 1-2 per 10000 pregnancies. The most common
diagnosis are von Willebrands disease & ITP.
Acquired causes: include anticoagulant therapy & consumptive coagulopathy resulting from
obstetric complications (such as pre-eclampsia, sepsis, abruption, amniotic fluid embolism).
Management: stop ongoing bleeding & replace blood products (include platelet,
coagulation factors & RBCs).


- Assess degree of blood loss & shock by clinical exam.
- Explore uterus & lower genital tract for evidence of tone, tissue or trauma.
- May be helpful to observe red-topped tube of blood no clot in 7-10 minutes indicates
coagulation problem.



Initial management of postpartum hemorrhage:
Early recognition of PPH, monitor vital signs, O
2
.
Establish IV access, place urinary catheter.
Baseline laboratory values, alert anesthesia & blood bank.
Correct hypovolemia with crystalloid.
Central hemodynamic monitoring (if indicated).
Correct anemia/coagulation disorders with blood products.
Medical therapy:
Oxytocin 20 U/L NS or RL IV connuous infusion in addion can give 10 U
intramyometrial (IMM) after delivery of the placenta.
Methylergonavine maleate (ergotamine) 0.25 mg IM/IMM q 5 min up to 1.25 mg
can be given as IV bolus of 0.125 mg (may exacerbate HTN).
Carboprost (hemabateTM) synthetic PGF-2 alpha analog) 0.25 mg IM/IMM q 15 min
to max 2 mg (major prostaglandin side eects & contraindicated in CV, pulmonary,
renal & hepatic dysfunction).
Local control:
Bimanual compression: elevate the uterus & massage through patients abdomen.
Uterine packing (mesh with antibiotic treatment).
Surgical therapy: (intractable PPH):
D&C (beware of vigorous scraping which may cause Ashermans syndrome).
Lapratomy with bilateral ligation of the uterine artery (may be effective), internal iliac
artery (not proven), ovarian artery, or hypogastric artery.
Hysterectomy (last option) with angiographic embolization if post hysterectomy
bleeding.

Pap Smear

Prepared by: Dalal Al-Omar


- Endocervical and exocervical cell sampling, Transitional Zone sampling..
- False posive 5-10%, False Negave 10-40%.
- Identifies Squamous cell carcinoma, less reliable for adenocarcinoma.
- Screening for all women start at age 21, or 3 years aer onset of vaginal intercourse.

- Women >30 years:-
*If 3 normal Paps in a row, and no previous abnormal Paps, can get screenend every 2-3years (if
adequate recall mechanism in place).

- Women >70years:-
*If 3 normal Paps in a row and no abnormal Paps in the last 10 years, can disconnue screening.

- Pregnant women and women who have sex with women should follow the routine cervical screening
regimen.

- Hysterectomy(according to type) :-

* Total hysterectomy: discontinue screening if hysterectomy was for benign disease and history of
cervical dysplasia or HPV infection.

* Subtotal hysterectomy: continue screening according to guidelines.

- Exception to guidelines:-
* Immunocompromized (Organ transplantation, steroids, DES exposure)
* HIV and high risk.
* Unscreened patients.






















Classification of Squamous Cell Abnormalities
You should know The Bethesda System ONLY
Description CIN Grading
Bethesda System
Class (outdated)
Normal Normal Normal Class I
Atypia Reactive or
Neoplastic
Atypia ASCUS (2) Class II
HPV HPV
Low-Grade SIL (3) Class II
Atypia with HPV
Atypia, "condylomatous atypia" and
"koilocytic atypia"
Low-Grade SIL Class II
Mild Dysplasia CIN I Low-Grade SIL Class III
Moderate Dysplasia CIN II High-Grade SIL Class III
Severe Dysplasia CIN III High-Grade SIL Class III
Carcinoma in-situ CIS High-Grade SIL Class IV
Invasive Cancer Invasive Cancer Invasive Cancer Class V
1. Kurman, R.J., Solomon D. The Bethesda System for reporting cervical/vaginal cytologic diagnoses,
Springer-Verlag, New York, 1994
2. ASCUS: Atypical squamous or glandular cells of undetermined significance should be qualified
further, if possible, as to whether a reactive or neoplastic process is favored.
3. SIL: Squamous intraepithelial lesion.













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Ob/Gyne Instruments







Used to visualize the cervix and vagina in cases of
1. Inspecon of cervix & vagina (pap smear, discharge, swab)
2. High vaginal swab
3. Conrm PROM
4. IUD inseron







Used to visualize the cervix and vagina for
1. Inspect vaginal wall for lesions (fistula, prolapse, neoplasm)
2. D&C
3. Exploration in PPH


1)
Prepared by: Salman Jan






Indications:
1.Fetal: distress, cord prolapse
2.Maternal:
*shorten the 2nd stage (cardic disease, pul.edema, hypertension, neurological dysfuncons)
*Maternal exhaustion
*Poor maternal effort
3.Elecve:
*After coming head in breech.del.
*During caesrean section

Pre-requisites:
- Fetal:
1. Head engaged ( staon +2 or lower)
2. Vertex or face presentation
3. Position of the fetus precisely known
- Maternal:
1. Cervice fully dilated
2. Membrane must be ruptured
3. No cephalopelvic disproporon
4. Bladder empty
5. Adequate analgesia & anesthesia
6. Generous episitomy
7. Lithotomy posion
8. Empty rectum

Contraindications are the opposite to them!

Complications:
- Fetal:
1. Facial n.or brachial pluxes injury
2. Skull fractures
3. Heamatoma (caput saccundum)
4. Intracranial Hmg
- Maternal:
1. Tear and laceration of the cervix
2. Rupture of bladder
3. Extension of episitomy
4. Bleeding
5. Infections





Types:
- simpson


- piper


- Kielland









Indications: Same as forceps.. PLUS few more points !

Prerequities:
Full term baby
Full flexion of the head
Sucon pressure < 600 mmHg
Not more than 3 applicaon
Dont twist the cup !

Contraindications:
1. Face or other than vertex presentation
2. Premature baby
3. Fetal coagulopathies
4. Fallowing fetal scalp sampling!

Complication:
1. Vaginal laceration and fistula
2. Fetal scalp heamatoma, laceration






Uses:
Obtain cytology smear form the cervice and vagina ( screening purposes)

Copmnants

- Ayre spatula (2 ends)




- Endocervical swab


- Fixator


- Slide







Use:
1.Obtain swab form any uid or discharge
2.High vaginal swab







Looks like a swab but has a yellow head ..
Used to confrim rupture of membrane: Alkaline aminotic fluid: Yellow >>>>> Blue




(internal moniter)







Uses:
Record fetal ECG by applying small clip to fetal scalp.





Indications:
1. Chorioaminois
2. Meuconium stained liquor
3. Twins
4. Excessive fetal movment
5. Unsasfactory CTG
6. High risk pregnancy

Advantages:
More reliable tracing to fetal heart beat & variability..

Disadvantages:
1. Rupture of membrane is a must; spontaneous or artificial
2. Little chance of infection; mother & fetus
3. Scalp trauma

Contraindictions:
1. Maternal infection e.g HIV, herpes simplex
2. Sever fetal coagulopathy




(ovum forcepse)
Curved


Stright



Uses:
1. Remove conceptional product, intrautrine, cervical polyp
2. To hold tissue e.g cervix during D&C











Use: non pharmacological induction of labor (Rupture membrane)

Complication:
1. Fetal & maternal injuries
2. Cord prolapse
3. Repture of vasa previa
4. Chorioaminoitis