ﻟﲪﺮﻦ ﺍﻟﺮﺣﻴﻢ ﺑﺴﻢ ﷲﺍ ﺍﻟﲪﺮ ﻧﳏ ﺎﻤﺪ... ﺍﻟﻠﻬﻢ ﺻ ﹼﻞ ﻭ ﺳﻠﹼﻢ ﻋﻠﻰ ﺳﻴﺪﻧﳏ ﺃﻋﺰﺍﺋﻲ ﻃﻼﺏ ﻭﻃﺎﻟﺒﺎﺕ ﻛﻠﻴﺔ ﺍﻟﻄ ـــــﺐ..،، ﷲﺍ ﻭ ﺑﺮﻛﺎﺗ ﻪ،، ﲪﺭﺔ ﷲﺍ ﺍﻟﺴﻼﻡ ﻋﻠﻴﻜﻢ ﻭ ﲪﺭ ﻣﳓﺎﺘـﺎﺝ ﱃﺇ ﻣـﻦ ﻳـﺪﻋﻤﻨﺎ ﻭ ﻳـﺪﻓﻌﻨﺎ ﱃﺇ ﺍﻷﻣـﺎﻡ ـﲑﺜﺍ ﻣﳓﺎ ﺧﻼﻝ ﻣﺮﺍﺣﻞ ﺣﻴﺎﺗﻨـﺎ ﳌﺍﺨﺘﻠﻔـﺔ ،،ﻛـﲑﺜ ﺰﲢ ﺓﺘـﻮﻱ ﺧﻼﺻـﺔ ﺃﳒ ﻥﺪ ﻣﺎﺩﺓ ﻋﻠﻤﻴﺔ ﺟﺎﻫﺰﲢ ﻣﻌﻨﻮﻳﺎﹰ ﻭﻋﻠﻤﻴﺎﹰ .ﻣﻦ ﲨﺃﻞ ﺍﻟﺪﻋﻢ ﺍﻟﻌﻠﻤﻲ ﺃﳒ ﲔﺒ ﺍﻟﺘﻄﺒﻴﻘﻲ ﻭ ﺍﻟﻨﻈﺮﻱ ﻟﰲ ﺐ ﳉﺍﺎﻧﻧﲔﺒ ﻋﺪﺓ ﻣﺮﺍﺟﻊ ،ﺗﺴﺎﻋﺪ ﺍﻟﻄﺎﻟﰲ MKS NOTEs IN Ob Ob/ /Gyn // / Gyn ﻭﻛﺘﺎﺑﻨﺎGy n "
ﺘﲎﻤ ﺍﱵﻟ ﻧﺘﲎﻤ ﻣﰲ ﺔ ﻛﻠﻴﺔ ﺍﻟﻄﺐ .ﻭﻫﻮ ﻫﺪﻳﺘﻨﺎ ﳌﺍﺘﻮﺍﺿﻌﻪ ﻭﺍﱵﻟ ﻫﻮ ﺩﻋﻤﻨﺎ ﻟﻜﻞ ﺍﻷﺟﻴﺎﻝ ﺍﻟﻘﺎﺩﻣﰲ ﺃﻥ ﻳﻜﻮﻥ ﻓﻴﻬـﺎ ﺍﻟﻨﻔـﻊ ﻭﺍﻟﻔﺎﺋـﺪﻩ ﻟﺰﻣﻼﺋﻨـﺎ ﺃﻃﺒـﺎﺀ ﳌﺍﺴـﺘﻘﺒﻞ .ﻭﻗـﺪ ﺑـﺬﻝ ﺍﻟﻔﺮﻳـﻖ ﺟﻬـﺪﻩ ﺎﷲ ﻝ ﻋﺰ ﻭﺟﻞ -ﻹﻏﻨﺎﺋﻚ ﻋﻦ ﻟﻜﺘﺎﺑﺔ ﳌﺍﻮﺍﺿﻴﻊ ﺑﺸﻜﻞ ﻣﺘﻜﺎﻣﻞ ﻗﺪﺭ ﺍﻹﻣﻜﺎﻥ -ﻭ ﺍﻟﻜﻤﺎﷲ ﺩﰲ ﺭ ﻣﺮﺣﻠﺔ ﻣﺎ ﻗﺒﻞ ﺍﻟﺘﺨﺮﺝ ﺍﻟﺘﺸﺘﺖ ﲔﺑ ﻋﺪﺓ ﻣﺼﺎﺩﰲ ﺑﰲ ﻪ ﺳﺠﻞ ﺃﻋﻤﺎﻟﻨﺎ... ﺃﳚ ﻥﻌﻞ ﻫﺬﺍ ﺍﻟﻌﻤﻞ ﻋﻠﻤﺎﹰ ﻳﻨﺘﻔﻊ ﺑﰲ ﻧﺴﺄﻝ ﷲﺍ ﺍﻹﺧﻼﺹ ..،،ﻭ ﺃﳚ ﻤﳍﺎـﺎ ﻟـﺬﺍ ﻣﺎﺯﻟﻨﺎ ﻧﻌﻤﻞ ﻋﻠﻰ ﺗﻄﻮﻳﺮ ﺍﻟﻄﺒﻌﺔ ﳉﺍﺪﻳﺪﺓ ﻟﺘﻐﻄﻲ ﳌﺍﺰﻳﺪ ﻣﻦ ﳌﺍﻮﺍﺿﻴﻊ ﻭ ﺇﻛﻤﳍﺎ ﻳﺴﺮﻧﺎ ﺍﺳﺘﻘﺒﺎﻝ ﻣﻼﺣﻈﺎﺗﻜﻢ ﻭ ﻣﺴﺎﻫـﻤﺎﺗﻜﻢ ﻛﺬﻟﻚ ﻭ ﺫﻟﻚ ﺑﺰﻳﺎﺭﺗﻜﻢ ﻭﺗﺸﺮﻳﻔﻜﻢ ﻟﻨﺎ www. www .mksforum .mksforum. mksforum .net ﰲ ﺑﻴﺘﻨﺎ "ﻣﻠﺘﻘﻰ ﺍﻟﻔﺮﺳﺎﻥ" ..ﻓﺮﺳﺎﻥ ﺍﻟﻄﺐ .ﻋﻠﻰ ﺍﻟﻌﻨﻮﺍﻥ .net
ﻴﰲ ﻖ ﺍﻟﺪﻧﻴﺎ ﻭ ﺍﻵﺧﺮﺓ ﺘﲎﻤ ﻟﻜﻢ ﺍﻟﺘﻮﻓﻴﰲ ﻧﺘﲎﻤ ﻧﰲ ﺎ ﺩﻋﻮﺍﺗﻜﻢ... ﻭ ﺍﺫﻛﺮﻭﻧﰲ
ﺑﺎﻟﻨﻴﺎﺑﺔ ﻋﻦ ﻓﺮﻳﻖ ﺍﻟﻌﻤﻞ ﻤﲞ ﺪﺎﺭﻱ ﳏﻤﲞ ﻛﻠﻴﺔ ﺍﻟﻄﺐ -ﺟﺎﻣﻌﺔ ﳌﺍﻠﻚ ﻋﺒﺪ ﺍﻟﻌﺰﻳﺰ
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, 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 3rd 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 pain………………………………………………………………………………………… 24 Amenorrhea…………………… …………………………………………………………………. 29 Infertility………………………………………………… ……………………………………….. 37 Ovarian cancer……………………………………………………………….……………………. 41 Cervical cancer……………………………………………………………………………………. 46 Gestational Trophoblastic Disease-GTD…………………………………………………………. 51 OBSTETRICS
Ovulation, Fertilization, Implantation and the t he Placenta………………………………… Placenta………………………………………….. ………..57 Diabetes Mellitus during Pregnancy………………………………………………………...……. Pregnanc y………………………………………………………...……. 67 Renal disease in pregnancy……………………………………………….……………………….. 72 Bleeding in 3rd Trimester (Antepartum Hemorrhage)………………… Hemorrhage)………………………….. ……….. ………... …… 75 - Placenta previa……………………………………………………………… ………… 75 - Abruptio Abrupti o placenta……………………………… placent a……………………………… …………………………… ……… 76 - Vasa previa……………………………………………………………………………….. 80 Miscarriage (Abortion)……………………………………………………………… ……………81 Intrauterine Fetal Death (IUFD)…………………………………………………………………. 83 Intrauterine Growth Restriction (IUGR)………………………… (IUGR)……………………………………… …………………………… ………………… … 86 Normal Labor & Dystocia………………………………………………………………………… 91 Induction & augmentation of labour……………………………………………………………… 96 Abnormal Abno rmal Labor & Delivery………………………………………………………………… ….100 - Labor Dystocia…………………………………………………………………………. 100 - Malpresentation………………………………………………………………………... 102 -- breech:……………………………………………………………… … … . ….102 --- External cephalic version (ECV)……………………… …………….. 102 -- Transverse (shoulder presentation) or oblique……………………… oblique……………………… … …...103 -- Other malpresentation………………………………………………… ………103 - Intrapartum complications:…………………………………………………………… ..104 -- Shoulder dystocia……………………………………………………………… 104 -- 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 smear……………………… ………………………………………………………………… 118 Ob/Gyne Instruments…………………………………………………………………………… 121
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
Superficial Inferior surface : Crura of clitoris 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 fro nt of piriformis muscle. - Branches to the pelvic muscles, m uscles, 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 nerves (S2,S3,S4) : sacral part parasymp 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 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 aort ic nodes
- Known as the vulva or pudenda - Innervated by pudendal nerve - Anterior to the vulva,innervations by ilio inguinal 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) The round ligament in IN - Uterosacral ligaments : condensation of endopelvic fascia , which FRONT FRONT of the the broad broad li ament insert into the posterior-inferior portion o f the uterus at the level of the isthmus.
- 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 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 interstitial - 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. th
•
5 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 undifferenated 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 s ource 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 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 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) majora) and urogenital folds medially (give rise to labia minora and prepuce 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 examination after intercourse 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 c ollecting 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 Arab’s 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 (5±2 days).
Blood loss not more than 80 ml/day.
Cycle length 21-40 days (30±2).
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 There’s monthly increase in FSH which stimulates the growth of primordial follicles. One develops, & ovulaon takes place on day 14 on the surge of LH. There’s 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 t he beating cilia in fimbriae. The follicles enlarge, but if there’s 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 c ycle. 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 don’t 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 fibrinolyc enzymes, & usually does not coagulate, thus it flows 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 cornified. 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 Late follicular phase (due to +ve feedback of E2, causes LH surge). At end of the cycle (due to –ve feedback of E2 & progesterone.
GnRH decrease Secretory phase (because of 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 suffer from it. Unknown etiology.
Clinical features:
-
Tension. Breast pain. GIT upset. Depression. Loss of control Irritability. Aggression. Insomnia.
Pelvic Mass Prepared by: 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 v ast & depend on the patient’s 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.
It could be discovered incidentally by obstetric examination or annual examination.
Differential diagnosis of pelvic mass Gynecological: Ovarian:
Functional cysts (always benign): •
Corpus luteum cyst:
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.
Other associated symptoms change in bowel habits, any gastrointestinal
o
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: differential:
A CBC with differential should be obtained t o 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 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) (laparoscopy)
•
Linear salpingostomy if tube salvageable.
•
Salpingectomy if tube damaged or ectopic is ipsilateral recurrence.
•
May require lapratomy
Medical: 2
•
Methotrexate 50 mg/m 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 don’t require treatment
Medical:
GnRH-a up to 6 months, shrink fibroid 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 lifethreatening 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 inflammato inflammatory ry 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 (McBurrey’s 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 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 culdesac, 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 Adenomyosis
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 o rgans 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 : 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 o nset (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: Infertility Hx of infertility is consistent with endometriosis or pelvic adhesions from o prior PID. PID pelvic adhesions or hydrosalpnix. o o Past gonococcal/chlamydial infection. o Endometriosis. o Time of the last pelvic exam. Past abortions. o OCP use. o 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. Genitofemoral L1, L2. o • 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).` NSAIDs. o o TCAs The following are potential options: Unilateral adnexectomy for unilateral pain. o TAH. o 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. 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 HYPOTHALAMIC : ↓ FSH/LH levels 1-Congenital lack of GnRH e.g. Kallman’s 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 Sheehan’s syndrome (Simmond disease) : Pituitary infarction from hypotension during postpartum hemorrhage. 2-Primary Hypopituitarism. 3-Tumors: adenoma, Craniopharyngioma, prolactinsecreting tumors. 4-Hemosiderosis: Iron deposition in pituitary that impairs its function.
OVARIAN : ↑ FSH/LH levels 1-Menopause. 2-Premature ovarian failure. 3-Savage’s syndrome: Ovarian resistance to FSH/LH 4-Enzyme defects: commonly 17α-hydroxylase. 5-Gonadal dysgenesis : Turner’s syndrome 45X 6-Chronic anovulation: Polycystic ovary syndrome PCOS, ovarian/adrenal tumor. 7-Radiation, chemotherapy.
Hormonal state HYPERGONADOTROOIC : 1-Turner’s syndrome 45X. 2-Premature ovarian failure. 3-Gonadal dysgenesis: XYgenotype, Swyer syndrome 4-Gonadal agenesis. 5-Resistant ovary syndrome (Savage’s syndrome). 6-Galactosemia: an autosomal recessive deficiency in galactose-1-phosphate uridyltransferase (toxic effect of galactose metabolites led to↓ oogonia. 7-Enzyme deficiencies: a- 17α-hydroxylase (prevent synthesis of sex steroid) have ovaries but not functioning, present with absent 2ndry sexual cha. , HTN, hypokalemia and ↑ progesterone level. enzyme. b- ↓ aromataze enzyme.
HYPOGONADOTROPIC HYPOGONADOTROPIC : 1-Anorexia (amenorrhea, bradycardia, 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. Kallman’s 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.
normal FSH/LH 1-Congenital mullerian (uterine/vaginal) agenesis (Mayer-RokitanskyKuster-Hause (Mayer-RokitanskyKuster-Hau se 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)
UTERINE :
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-RokitanskyKusterHause 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…
- Breasts are an endogenous assay of ESTROGEN. - Pubic & axillary hair are an endogenous assay of ANDROGEN. - When diagnose amenorrhea, always role out PREGNANCY first.
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 seco ndary amenorrhea. * Imperforate Hymen & Transverse Vaginal Septum: three degrees are recognized…
_____________ *Gynecology illustrated
-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 (RokitanskyKuster-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.
- 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
Second most common cause of primary amenorrhea
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) ( 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 no ted, 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:
- 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 breast & puberty development and linear growth.
Differential diagnosis is gonadal dysgenesis (Turner
syndrome) and hypothalamic-pituitary failure.
* FSH level and karyotype help make the diagnosis.
Gonadal failure (Hypergonadotropic (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.
Turner syndrome is the Single most common cause of primary amenorrhea, accounting for >50% of gonadal failure paents.
- Short status, webbed neck, cubitus vulgas, infantile genitalia, c oarctation 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 (17α-hydroxylase). - Management: Estrogen and progesterone replacement for development of the secondary sexual characteristics and prevent osteoporosis.
Hypothalamic-pituitary Hypothalamic-pituitary failure (Hypogonadotropic (Hypogonadotropic Hypogonadism): Hypogonadism):
- No secondary sexual characteristic but uterus present by ultrasound. - FSH levels will be low. low. A - HYPOTHALAMUS: HYPOTHALAMUS: stress, anxiety, anorexia nervosa, excessive exercise, tumors, TB, sarcoidosis, congenital (KALLMAN's (KALLMAN's SYNDROME) SYNDROME) : -
Insufficient GnRH production and also anosmia & color blindness.
-
X- linked,
-
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.
male > female.
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.
Breast (-) (+) (+) (-)
Uterus (+) (+) (-) (-)
st
1 common(Gonadal failure, Hypothalamic-pituitary failure) nd Rare (same workup as 2 amenorrhea) Common(Mullerian agenesis, androgen insensitivity) Very Rare , almost always 46,XY
Breasts present, uterus absent Cause of Uterus absent? Estrogen source Pubic hair Testosterone level
Mullerian Agenesis (46,xx) Idiopathic Ovaries Present Female
Androgen Insensitivity (46.xY) MIF Testes Absent Male
Breasts absent, uterus present FSH Why No estrogen Ovaries? Diagnostic test
Gonadal Dysgenesis (4S.x) ↑ No ovarian follicles "Streak"
HPAxis Failure (46,xx) ↓ Follicles not stimulated Normal CNS imaging
-
Secondary Amenorrhea Is the cessaon of menses for 6 months or a three-cycle interval in women who have been menstruating regularly. - Pregnancy is the most common cause of Prevalence: 4-5% of women (excluding pregnancy)
secondary amenorrhea. - When diagnose amenorrhea, always role out PREGNANCY first.
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 stimulatio n 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. - Sheehan’s 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).
-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 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. 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. etio logy.
An elevated FSH : suggests ovarian failure or A low FSH : - suggests -
Savage
hypothalamic-pituitary 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: EPCT: - Absence of withdrawal withdrawal bleeding bleeding is diagnostic of an of an outflow tract obstruction or endometrial 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 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, D HEA, 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 (P CaS) • 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 characteristics of benign vs. malignant ovarian tumors: Benign
< 8-10 cm in diameter unilateral Cystic Uniloculated Thin septations No ascites
Malignant
>10 cm in diameter Bilateral Solid elements (internal papillary structures/mural nodules) Mutiloculated Thick septations 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 ov ulation 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
Prognosis: (5 years survival)
Stage I: 75-95% Stage II: 45-65% Stage III: 20-40% Stage IV: 10-15%
Classification of ovarian cancer Germ cell tumor 5-7\%
Epithelia ovarian tumor 87-90%
Classification of ovarian cancer
Sex cord stromal 5-7%
Metastatic ovarian cancer 4-8% Epithelial ovarian cancer: Origin Arise from coelomic epithelium (i.e. the mesothelium). • • This epithelium also give rise to peritoneum & the paramesonephric (müllerian duct), which explains the histologic similarities between lesions of ovarian, peritoneum, & urogenital tract. Types: • Serous (50-70%) 20-30 bilateral o Mucinous (10-15%) • Rarely complicated by pseudomyxoma peritonei. o Implants seed abdominal cavity & produce large quantities of mucous. o 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%). The median age at diagnosis is 17 years. o Lactate dehydrogenase may be a useful tumor marker. o o Overall long-term survival is 85%. Endodermal sinus tumors: • Are the second most common type. o 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: • Are the most common type (70%). o o 95% are stage at diagnosis & unilateral. o Estrogen producing feminization effects (precocious puberty, menorrhagia, postmenopausal bleeding). Sertoli-leyding tumors: • o Are rare & frequently presented with signs of hyperandrognism as it’s 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. There’s 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 benefit 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 first degree relave affected, 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 + churchill’s pocketbook – Obstetrics & Gynecology + eMedicine website + Dr.Sait’s 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 direc tly. 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 ri sk) 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. Q: What colposcopic findings are suggestive of cervical cancer? A: 1) Abnormally branched, looped, or punctuated blood vessels (secondary neovascularization of the tumoe & distortion of the blood vessels by the growing mass). 2 Abnor Abnormal mal a earanc earance e of the the surf surface ace of the the cervi cervix. x.
to
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 ³ stage IB2.
Clinical staging Stage
Description
Cancer is confined to the cervix & identified only microscopically microscopicall y 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. Cancer is confined to the cervix c ervix & larger than stage 1a-2 OR associated with a visible Ib lesion. Stage Ib-1: up to 4.0 cm cervical tumor diameter. Stage Ib-2: > 4.0 cm cervical tumor diameter. Involvement of the upper 2/3 of the vagina, but no evidence of parametrial IIa involvement. Infiltration of the parametria but not out to the sidewall. IIb Involvement of the lower 1/3 of the vagina but not out to the pelvic sidewall if the IIIa parametria are involved Extension to the pelvic sidewall &/or hydronephrosis or non-functional kidney IIIb (unless known to be attributable to other causes). Extension outside the reproductive tract with involvement of the mucosa of the IVa bladder. Distant metastases IVb Cervical cancer prognosis (5 years survival figures): Stage I: 85-90% Stage II: 60-75% Stage III: 35-45% Stage IV: 15-20% Ia
• •
• •
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 vaccine (Harper 2004) for for types 16/18(100% efficacy) efficacy) Merck vaccine (villa 2005) for types 6/11/16/18 6/11/16/18 ( 88% efficacy (RCT PLACEBO) 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 o Storage: 2-8 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 Prepared by: by: Salman Jan Sources: Toronto Notes + Tarek Arab sheet
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)
GTD Hydatiform mole Complete mole
GTT
Invasive mole
Partial mole
PSTT
Choriocarcinoma Non-Metastatic Low Risk High Risk
PSTT = placental site trophoblastic tumor
Hydatidiform moles Incidence o o
Japan has highest incidence – 2/1000 pregnancy Europe & north America – 0.6 – 1.1 pregnancy
Types o o
Partial & Complete
metastatic
-
Chromosomal origin:
-
Complete Vs. Partial: Complete
Risk factors
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
Pathological characteristic
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
Patrial 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 Some of chorionic villi are swollen & some are normal o Contain some fetal blood vessels v essels in chorionic villi o Hyperplasia in only synsetiotrophblast o Fetus can be seen or fetal membrane or fetal parts
Clinical Pictures
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 & nonpitting edema" o Hyperthyroidism
Signs
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
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 & nonpitting edema" o Hyperthyroidism o Hx. Of IUGR & abortion
o small of date o Vaginal Ex. >>> passage of vesicles o Pre-eclampsia o Hyperthyroidism o Ovarian cysts rare o Fetal parts
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 intrauterine hemorrhage BhCG If complete: abnormally higher than 80000 mlU/ml If partial: not very hight
o
o
Treatment o o o
o
suction evacuation followed by curettage & follow up: admin oxytocin during curettage to stimulate uterine contravtion BhCG level should steadily decline aer evacuaon to undetected level by 16 week, if it still rise, think of either recurrence or pregnancy if recurrent after evacuation, chemotherapy required, the drug used is Methotrexate
Follow up o o
o
contraception to avoid pregnancy during follow up period 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 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 st In 1 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 PSTT Invasive moles
o o
-
Invasive Mole o
o o o o
-
PSTT: o o o o o o o o
-
Diagnosis made by rising or a plateau in BhCG development of metastases following treatment of documented molar pregnancy Histology – molar tissue Invade locally >>> myometrium, serosa & vagina Metastases are rare Management: hysterevtomy, don't respond to chemotherapy
Occur in plasental site Tumor marker is HPL Can metastasis Rare aggressive form of choricarcinoma Abnormal growth of intermediate trophoblastic cells Low BhCG, production of hPL, insensitive to chemotherapy Poorly respond to chemotherapy Management: hysterectomy but inmetastasis (hysterectomy + chemotherapy)
Choricacinoma: o o o
Often present with symptoms from metastases Highly anaplastic, highly vascular 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:
o
Clinical pictures: Abnormal bleeding Secondary post partum hemorrhage Abortion Ectopic pregnancy
-
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
Ovulation, Fertilization, Implantation 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 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 the primary follicle. 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. oophorus.
Mature follicle 10 mm or more in diameter Surrounded by theca interna (steroid secretion rich in blood v esseles) and the theca externa , that merges with the ovarian stroma.
Graafian follicle:
Before ovulation:
st
Primary oocyte resumes 1 meioc division, resulng in 2 daughter cells (haploid),
these are the secondary oocyte and first and first polar body . 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 premenstrual 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 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 rd
Fusion---zygote---blastomeres---3 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, 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 t raverse 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 : 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 and when lined by mesoderm mesoderm
becomes the extraembryonic coelom •
th
On 17 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 a s the (levae). rd
Aer 3 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
th
At 4 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 a re replenished 3-4 mes per minute Placental membrane : separate maternal 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 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 depression on 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 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 : st
•
1 trimester : Ultrafiltrate of maternal plasma
•
Later : Transudation of foetal plasma across the foetal skin
•
12-24 week: Foetal urine contributes to it
•
Other sources : Foetal secretion from the GIT and respiratory tract and transudate across the
th
umbilical cord At term , 700-1000 ml of amnioc fluid is exchanged every 24 hrs Oligohydramnios : •
Marked deficiency in deficiency in volume of amniotic fluid
•
May produce foetal hypoxia
•
Associated with intrauterine growth retardaon in 60% cases
Polyhydramnios Polyhydramnios : Excessive volume , usually usually exceeding 2 L Complications 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 – 6th 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
GDM definition is: NOT related to specific date e.g. aer 20 weeks NOT related to Persist/not persist after pregnancy
1. DM I : no insulin due to pancreatic damage - require external insulin 2. DM II : insulin resistance - require life style modification 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. Maternal insulin is rising, wouldn’t the fetal have hypoglycemia ? Answer is : NO, maternal insulin does not cross placenta
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 1. 2. 3. 4. 5.
Family Hx of DM Past Hx of GDM Age extremes : <20 & >35 Obesity Mutiparity
Past Pregnancy History 6. 7. 8. 9.
Hx of Recurrent abortion Hx of unexplained IUFD Hx of Anomalies Hx of Macrosomia
Current Pregnancy History 10. 11. 12. 13.
Persistent GlucosUria PolyHydramenious Fetus large-for-date Hx of Macrosomia
IUGR is NOT an indication for Screening
1. S/S of DM : thirst, polyphagia, increased Wt gain, polyuria (hard to distinguish cause it’s a pregnancy symptom) 2. Fetus is BIG-FOR-DATE
I am suspecting my patient to have GDM .. how to diagnose ? 1. Low risk ? do GCT (Glucose challenge test) How to do ? Pregnancy is at week 24 (maximum insulin resistance & starng hPL) o 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 ? st o Do it in 1 Ante-natal visit. If normal, repeat at week 24 o Paent takes 100g glucose 12 hours fasng – no smoking & caffeine of 3 days o Record glucose level at (fasng), (aer 1 hour), ( aer 2 hours), (aer 3 hours), o
•
Normal readings (O’Sullvian criteria) no more than : o 5.8 mmol (105 mg) Fasting : 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) o Abnormal readings ! 1 reading abnormal : impaired GTT = paent is high risk to develop GDM o 2 readings abnormal : paent has GDM o
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 1. Congenital Anomalies 2. Abortion Mainly DM I unlikely if GDM
1st Trimester 1. PolyHydraminious 2. Mal Position & Presentation 3. Abnormal placenta implantation
2nd & 3rd Trimester 1. Macrosomia 2. PROM
In labor 1.Sholder 1. Sholder dystocia 2.PPH 2. PPH 3.Cesarean 3. Cesarean Section
Neonatal 1. Hypoglycemia 2. RDS 3. Neonatal Jundice 4. Kernictrus
Maternal specific 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 :
: ﺩﻋﻮﻧﺎ ﻧﻔﻜﺮ ﻣﻨﻄﻘﻴﺎﹰ ،Complicationsﻟﻨﻔﻬﻢ ﺍﻟـ :ﻣﻦ ﺑﺪﺍﻳﺔ ﳊﺍﻤﻞ ! Congenital Anomalies ﺗﺴﺒﺐ.embryogenesis ﲔﻨ ﳉﺍﲔﻨ ﻟﰲ ﻚ ﺑﺪﺍﻳﺎﺕ ﺧﻠﻖ ﳉﺍ ﻭ ﺫﻟﰲ،،Hyperglycemia .Abortion ُﺃﻥ ﺍﻟﺘﺸﻮﻫﺎﺕ ﳋﺍﻠﻘﻴﺔ ﻏﺎﻟﺒﺎﹰ ﻣﺎ ﺗﺆﺩﻱ ﱃﺇ ﺇﺳﻼﺏ ﳓﻧﻭﻌﻦﻠﻢ ﺳﻠﻔﺎﹰ :ﺧﰲ ﻞ ﻧﺪﺧﰲ.. ﻭ ﻣﺸﻲ ﳊﺍﺎﻝ ، ﱂ ﻳﺘﻢ ﺇﺳﻼﺏ،ﻃﻴﺐ :1
st
Trimester
ﺳﺘﺆﺩﻱ ﱃﺇ ،Fetal polyuria Mal Position & Presentation ﻗﺪ ﺗﺆﺩﻱ ﱃﺇPolyHydraminious Previa = Abnormal placenta implantation ﻗﺪ ﺗﺆﺩﻱ ﱃﺇAbnormal Presentation PolyHydraminious
:2
nd
rd
& 3 Trimester
ﺳﺘﺆﺩﻱ ﱃﺇ ،fetal hyper-insulinemia ﻭHyperglycemia ﺎ ﻭ ﺗﺒﻌﺎPROM ﻭ ﻫﺬﺍ ﻗﺪ ﻳﺆﺩﻱ ﱃﺇuterine-over-distention ﺳﺘﺆﺩﻱMacrosomia ﻭPloyHydraminious Macrosomia
:During Labor PPH = Uterine Atony ﻫﺬﺍ ﺑﻜﻞ ﺑﺴﺎﻃﺔ ﻳﺴﺒﺐ ، uterine-over-distention ﺳﺒﻖ ﻭ ﻗﻠﻨﺎ ﻭ ﻗﺪ ﻧﺪﺧﰲ ،Sholder dystocia ﻫﺬﺍ ﺑﻜﻞ ﺑﺴﺎﻃﺔ ﻳﺴﺒﺐ ،Macrosomia ﺳﺒﻖ ﻭ ﻗﻠﻨﺎ brain ﻭhypoxia ﺧﰲ ﻞ damage Higher Incidence of Cesarean
ﻫﺬﺍ ﺑﻜﻞ ﺑﺴﺎﻃﺔ ﻳﻌﻄﻴﻨﺎ ،Mal Position & Presentation ﺳﺒﻖ ﻭ ﻗﻠﻨﺎ Section
:Neonatal period Neonatal Hypoglycemia Hypoglycemia ﻫﺬﺍ ﺑﻜﻞ ﺑﺴﺎﻃﺔ ﻳﺴﺒﺐ ، fetal hyper-insulinemia ﺳﺒﻖ ﻭ ﻗﻠﻨﺎ ﻭ ﻳﺘﺮﺗﺐ ﻋﻠﻰDelayed organ maturation ﻫﺬﺍ ﺑﻜﻞ ﺑﺴﺎﻃﺔ ﻳﺴﺒﺐ ، ﺃﺛﻨﺎﺀ ﺍﻟﻨﻤﻮHyperglycemia ﺳﺒﻖ ﻭ ﻗﻠﻨﺎ :ﺫﻟﻚ Delayed lung maturity : RDS Delayed liver enzymes maturity : Neonatal Jundice .ﺴﲔﻜ ﲔﻨ ﳌﺍﺴﲔﻜ ﳉﺍﲔﻨ ! ﻭ ﻳﺆﺫﻱ ﻣﺦ ﳉﺍKernictrus ﻧﻔﺴﻬﺎ ﻗﺪ ﺗﺆﺩﻱ ﱃﺇJaundice -
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 HBA1C : during first visit. o Stop OHG drugs : they cross placenta (teratogenic & fetal hypoglycemia) Normal diet for any pregnant women women = 1800 kcal/day (36kcal/kg/day) o Advise patient to have glucometer (monitor blood glucose daily). o o
For follow up during visits : do 2 Point 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: st 1 Trimester : 0.6 units x ideal weight nd 2 Trimester : 0.7 units x ideal weight rd 3 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) NPH) • •
•
•
Fetal Well-being: BPP & NST. o 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 If Glucose level >8 mmol, use 2/3 of pre-pregnancy insulin insulin dose. o DM I : No insulin required during next 38-72 h o 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 Incidence: 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 mo nthly 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 1% >> hypovolemia . • more than 3%>>tubular damage Urine osmolality > 500 mOsm/L •
100.. less than
×
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 insufficiency (serum creanine level, <1.5 mg/dL) - Moderate renal insufficiency (serum creanine level, 1.5 -2.4 mg/dL) progressed to ESRD - Severe renal insufficiency (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 3rd Trimester ( Antepartum Antepartum Hemorrhage ) Prepared by: Sameerah Albugami – 6th year medical student (completed by Wafaa Al-Ahmadi) Source: Hacker + Toronto notes 2008 + Obstetrics & Gynecological Recall + Tarek Arab’s sheets.
Bleeding at third trimester or vaginal bleeding from 20 weeks to term. Incidence: 4%
Placental Placenta previa Placenta abruption Vasa pravia
Uterine Uterine rupture
Cervical Cervivitis Cervical erosion Cervical Ca
Vaginal Trauma Infection
Bleeding tendency Clotting disorders 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.
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.
Pathopyhysiology: Bleeding occur as a result of the disruption of the placental attachment secondary to the rd development & thinning of the uterine lower segment in the 3 trimester. Presentations: History: rd - Painless bright red vaginal bleeding in the 3 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. 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 c ommon). 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 1)Stabilize the patient: large IV with hydration & O2. 2)Maternal 2)Maternal Monitoring vital signs, CBC (for degree of bleeding), urine output, coagulation profile. 3)Fetal 3)Fetal monitoring NST, BPP, U/S. 4)Cross 4)Cross matching 4 units & blood product available. 5)Give 5)Give the mother rhogam if mother is RH negative. 6)If 6)If GA<37 weeks: Excessive bleeding or fetal distress perform C/S regardless of the GA. Minimal bleeding expectant management. 7)If 7)If GA>37 weeks and large bleeding delivery by C/S. If the placenta is 2 cm from the cervix; it is save to deliver vaginally.
لا ا ال 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.Sma’a Nather said we will perform high transfers C/S & never perform classical type, BUT Dr.Ramadani said we will perform classical type !!!
Definitions: Premature separaon of normally implanted placenta aer aer 20 weeks gestaons. Incidence: 0.5_1.5% Etiology: Idiopathic Risk factors: Maternal:
1) 2) 3) 4) 5) 6) 7)
Past Hx of abruption placenta. Maternal hypertension. Cigarette smoking. Multiparity. Increase maternal age. Uterine anomalies ,fibroid Trauma.
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. Blood may dissect towards uterine fundus concealed hemorrhage. OR extends downward towards cervix revealed hemorrhage. But the most common is mixed
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. - 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.
Presentation is divided into mild, moderate & sever: Mild Moderate 25% of placenta bed 25-50% of placenta bed separated separated Abdominal pain Gradual Mild tenderness on Ex Rigid, tender uterus Firm uterus Continuous, sever abdominal pain Minimal per vaginal loss Moderate to sever per vaginal blood loss No fetal distress Fetal distress Mother is stable
Complication: Fetal:
1) 2) 3) 4) 5)
Fetal distress. Fetal death (35% perinatal mortality). Prematurity & its complications. IUGR. Neurological sequale e.g. cerebral palsy.
Sever 50% of placenta bed separated Sudden Sever abdominal pain Moderate to absent bleeding
Fetal distress/demise of fetus Maternal hypovolaemia, shock, oligorrhea, DIC
Maternal:
1) 2) 3) 4) 5) 6) 7) 8) 9) 10)
Maternal mortality. DIC (20% of cases). Acute renal failure. Renal tubular acidosis. Anemia. Hemorrhagic shock. Shehan’s syndrome. Amoniotic fluid embolus. Ischemic necrosis of the distant organs. 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 there’s fetal distress or maternal hemodynamic instability} 9) In case of moderate to sever abruption: Vaginal delivery if no fetal distress If there’s fetal distress or materal hemodynamic instability deliver by C/S. 10) In case of dead fetus induce labor. Recurrence is 10% aer 1 abrupon , 25% aer 2 abrupons.
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
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 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. 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 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). Toxoplasma). - Smoking, Alcoholic. - Sudden physical or emotional shock. - Cervical Incompetence (the most common cause of aboron in 2nd trimester). The diagnosis is usually made when a mid-trimester mid-trimester pregnancy is lost with a clinical clinical picture of sudden unexpected rupture of the membranes, followed by painless painless expulsion of the products of conception. - Uterine Adhesion; synechiae or Asherman's $. st - Uterine Abnormalities; congenital or acquired (associated with pregnancy loss in both the 1 & the 2nd trimester). 2- Fetal Factors; Severe congenital anomalies either Genetics or morphological anomalies. anomalies. st
3- Chromosomal Factors; (the most common cause of aboron in 1 trimester)
Either Genetics or Morphological Abnormalities . 4- Immunological Factor; as Rh-Incomatability. 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 defined as expulsion of fetal ssue < 5 00 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
TORCH=Toxoplasmosis , Other infections
Rubella, CMV, Herpes simplex Other infections = Hepatitis B, Syphilis, Varicella-Zoster Virus, HIV
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).
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 co unseling 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 abo ve changes, give fresh frozen plasma & deliver.
2) Induction of labour: th
a) 20-28 week: 20 mg q3hrs prostaglandin E2 suppository (vagina) OR misoprostol Risks of prostaglandin E2: Uterine rupture Laceration Side effects of prostaglandin E2: Nausea, vomiting, diarrhea, pyrexia. Contraindications: Previous C/S, previous myomectomy, bronchial asthma, acute pulmonary disease.
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b) > 28 week: Oxytocin if no contractions & favorable bishop’s score Smaller doses of E2 due to risk of uterine rupture if the induction of the labour was contra Laminaria to ripen cervix. 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.
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- Infant weight < 10 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, dwarfism. 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 ( 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). •
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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 Q: how dose congenital infection affect fetal growth? ? HIV A: by interfering with cellular development; generally, the earlier the infant infected, the more sever the outcome. ? 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
1) 2) 3) 4) 5)
Changing in antepartum fetal testing reflect the pathophysiology changes (in sequence): Umbilical systolic/diastolic ratio increases as placental vascular resistance increases. Fetal growth on U/S slow or stops. Oligohydramnios develops due to diminish perfusion of t he fetal kidneys. Loss of fetal heart rate variability v ariability ± decelerations. Fetus dies.
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 TO RCH 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. Q: what is the fundal hight lag? A: a fundal hight smaller t han fetal gestational age.
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 t he 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. •
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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.
Placenta grade:
Q: what indices are evaluated in placental grading? A: placental calcium deposited & indentations in the chorionic plate. o o o
o
Grade 0: NO calcifications & NO indentations in the chorionic plate. Grade 1: Few calcifications throughout the placenta. Grade 2: Calcifications along the uterine wall & indentations in the chorionic plate. Grade 3: significant calcium deposits & indentations in the chorionic plate that appears to outline individual cotyledons.
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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.
Q: What are the most useful U/S criteria for determining IUGR? th A: EFW below 10 percentile, decreased AFW, elevated HC/AC.
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 flow 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
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 - 6th year student - 2008 Sources: OB Recall – Toronto Notes 2007 – Baby pink sheets – Clinical sessions
It’s 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. • 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)
Definitions you should know: • etal long axes to maternal long axes (longitudinal, transverse). Fetal Lie : relation of f etal • 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)
st 1. 1 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-
nd 2. 2 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. rd
3. 3 Stage : starting from expulsion of FETUS, till expulsion of PLACENTA. o Duraon: no more than 30 min (prime/mul) th 4. 4 stage: first 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) • •
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1 stage (cervical dilatation & descent): Maternal Care
Fetal Care
Any comfortable position, common is lateral recombent
Monitor fetal Heart Every 30 min Every 15 min if high risk • •
Orders : NPO IV fluids (ringer lactate) Empty bladder Fecal enema NaPO4 Shave & clean Pubic and vulvar area Insert IUPC (intra uterine pressure catheter) if ROM (rupture of membranes) occur • • • •
How to monitor ? CTG –most important Doppler – with each contraction Feto-scope • • •
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Vaginal Examination every 2 hours to check : Cervix (Bishop score) -see induction of laborMembrane : intact/rupture Fetal head molding Pelvic adequacy •
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Analgesia : Systemic o Pethidin 50-100 mg / 2-3 hours o IV /IM Regional o Epidural / Spinal Inhalation o N2O (50% Nitrox oxide + 50% O2) •
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Amniotomy if the method of Inducon / Augmentaon during stage 1
2nd stage (Delivery of fetus): Maternal Care Lithotomy position. Increases lumbosacral diameter
Fetal Care Monitor fetal Heart Every 15 min Every 5 min if high risk • •
With each contraction, tell mother to bear down. Rest between contractions.
Ritgen’s maneuver Hand behind rectum making UPWARD pressure Hand over fetal occipit making DOWNWARD pressure Used to guide the expulsion prossess. •
Episiotomy : Surgical incision in perineum Preformed when the presenting part separates the 2 labia apart by 4 cm or more. It is done to: Increase vulvar outlet o diameter o Prevent lacerations & tearing (read below) o Prevent relaxation of pelvic floor Indications o Primigravida o Breech presentation Shoulder Dystocia o Instumental delivery o Types Midline o Mediolateral o o J-shaped • •
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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 •
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Lacerations Grades: st 1 grade : vaginal mucosa / skin nd 2 grade : vaginal wall / perineal muscles rd 3 grade : reached Anal sphincter th 4 grade : involved rectal mucosa • •
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Nucule ? (ة ر) 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 Replace baby’s clamp by plasc 2 o cm away from abdomen. o Cut within 30 sec. Earlier = anemia Later = jaundice
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3 stage (Expulsion of PLACENTA): Maternal 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 o f placenta plac enta -----------------------------------------------------------------------> After placenta delivery : Fundal massage • • Oxytocin 20 units IV
Placental Care 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 No bleeding ? wait up to 1 hour o Bleeding ? do manual removal o under general anesthesia.
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4 stage (firt 1 hour post-partum): Monitor: Vitals • • Uterine involution : should be at level of umbilicus If above uterus, what do you call it ? Sub-involuted uterus (causes are same of uterine o atony) • Lochia Repair lacerations • Examine cord for: Missing vessel (30%) • associated with anomalies o mainly RENAL anomalies o 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.
Induction of labour is indicated when the risk of continuing pregnancy exceeds the risk associated with induced labour & delivery.
Absolute indications Maternal indications: Preeclampsia/eclampsia Maternal medical problems (DM, chronic renal failure, chronic pulmonary disease)
Relative indications Maternal indications: Chronic HTN Pregnancy induced HTN Gestational diabetes Logistic factors Risk of rapid labour Distance from the hospital Psychosocial indications Fetal indications PROM Fetal macrosomia Fetal demise Previous stillbirth Fetus with a major congenital anomalies Utero-placental indications: unexplained oligohydramnios
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Fetal indications: Chorioamnionitis Abnormal antepartum testing IUGR Post-term pregnancy (>42 weeks) isoimmunization Utero-placental indications: placenta abruption
Absolute contraindications Maternal contraindications: Active genital herpes Serious chronic medical conditions & unstable maternal conditions Fetal contraindications: Mal-presentation Fetal distress Premature fetus without lung maturity Utero-placental contraindications: Placenta previa Vasa previa Prior “classical” C/S
Relative contraindications Maternal contraindications: Cervical carcinoma Pelvic deformities
Fetal contraindications: Extreme macrosomia gross cephalo-pelvic disproportion
Utero-placental contraindications: Low-lying placenta Unexplained vaginal bleeding Cord presentation Myomectomy involving the uterine cavity
Confirm indication of induction. Confirm gestational age. Patient’s 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
Consider the following before induction: • Indication for induction • Contraindications • GA • Cervical favorability • Fetal presentation • Potential for CPD • Fetal well-being/FHR • Membrane status
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 confirms 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 Position Consistency Effacement (%) Dilatation (cm) Station of fetal head
0
1
2
3
Posterior Firm 0.30 0 -3
Mild Anterior 40-50 1-2 -2
anterior Soft 60-70 3-4 -1 or 0
>80 ≥5 +1
Failure to achieve labour &/or vaginal birth. Uterine hyper-stimulation & fetal compromise. Uterine rupture. Uterine atony & PPH. Maternal side effects to medications.
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). •
- 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.
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: TM Oxytocin (pitocin ): 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. Oxytocin t1/2 = 3.5 min • 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.
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 contractio n 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 leopoid’s 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 v ertex 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 midpelvic 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; Klumpke’s 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 (MecRobert’s 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 McRobert’s 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.)
Cervical incompetence is premature cervical dilation but in the absence of contraction before term..
• • •
7-10% of all deliveries. 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) 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\ 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 o f 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 Local:(uterine and cervical cause) Congenital: septate, unicornuate or bicornuate Traumatic: incompetent cervix,, excessive enlargement (hydramnios), use of IUD. Inflammatory: asherman’s
Neoplastic: leiomyomas • Maternal-fetal: 1. Placental anomalies. 2. PPROM (30-35% (30-35% of all preterm birth) 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% effaced.)
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.?
Conditions should be ruled out in preterm labor: 1. 2. 3. 4. 5. 6. 7.
PPROM Placental abruption Placenta previa Fetal death Infection Multiple gestation Fetal anomalies
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 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 distress/demise, ruCR, multiple gestation (relative)
anomalies,
fetal
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 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) • • • •
•
•
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 goo d outcome after delivary.
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
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
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 chorionicdecidual 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 • • •
Placental-vascular pathway(PVP-1) 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.
Stress-strain pathway
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 o nset of labour. - preterm premature ROM (PPROM): rupture of membranes before 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.
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. •
• 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
Organisms have been linked to PROM: • Ureaplasma urealyticum. Trichomonas vaginalis. • • Bacteroides species. • Chlamydia trachomatis GP B streptococcus (GBS) • • Gardnerella vaginalis and others.
In +Ve culture : Unknown whether result of : • Infection causing PROM through weakening of the membranes. Or • PROM leading to colonization with
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 tenderness - fluid properties change (color,smell,consistency) - Leukocytosis - cultures +ve
• 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. •
•
gush of fluid : - Water-thick - clear - continuous : wrench cloths - increase gush with cough (valsalva manuver) - no smell (changes in these properties could indicate infection)
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. 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.
Fetus\neonate 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)
mother 8. Chorioamnionitis 9. Endomyometritis 10. Puerperal sepsis
(complication of infection) infection)
Preterm PROM: The risk are primarily related r elated 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.
Active treatment: Close observation for infection. Antibiotic are given for variable periods according to duration of pregnancy.
< 24 weeks
Conservative ttt Active ttt (termination of pregnancy)
•
•
26-34 weeks
34-36 weeks
(poor outlook due to pulmonary hypoplasia)
The predominant complication is RDS
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-Corticosteroid (predinsolone) - Antibiotic. Consider tocolysis for 48h to permit administration of steroids if PPROM. Indicated if: - Infection is developed. - Maturity is reached - Labour is started.
"grey zone" where risk of death from RDS and neonatal sepsis is the same. ---------
Treatment of Choice.
if the labour dosen't start with 48h *ttt with ampicillin administration
>36 weeks the risk of death from sepsis is greater
-----------
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 P ROM 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 first 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 first 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 laceratio lacerations: ns: • 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). Placenta acreta is the most common type o Penetration through myometrium (percreta). of abnormal placentation occurring in
around 1 in 2500 deliveries. •
Risk factors: prior uterine surgery, placenta previa, smoking, & grand multiparity.
7-Coagulopathy: • Congenital coagulopathy: complicate 1-2 per 10000 pregnancies. The most common diagnosis are von Willebrand’s 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).
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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 effects & contraindicated in CV, pulmonary, renal & hepatic dysfunction). Local control: Bimanual compression: elevate the uterus & massage through patient’s abdomen. Uterine packing (mesh with antibiotic treatment). Surgical therapy: (intractable PPH): D&C (beware of vigorous scraping which may cause Asherman’s 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 Bethesda System
Description
CIN Grading
Normal
Normal
Normal
Class I
Atypia
ASCUS (2)
Class II
HPV
HPV
Low-Grade SIL (3)
Class II
Atypia with HPV
Atypia, "condylomatous atypia" and Low-Grade SIL "koilocytic atypia"
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
Atypia Reactive Neoplastic
or
Class (outdated)
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 Instrument Instrumentss Prepared by: by: Salman Jan
Used to visualize the cervix and vagina in cases of 1. Inspecon of cervix & vagina (pap smear, discharge, swab) 2. High vaginal swab 3. Confirm PROM 4. IUD inseron
Used to visualize the cervix and vagina for 1. 1.Inspect Inspect vaginal wall for lesions (fistula, prolapse, neoplasm) 2. D&C 3. 3.Exploration Exploration in PPH
1)
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. 1.Head Head engaged ( staon +2 or lower) 2. 2.Vertex Vertex or face presentation 3. 3.Position 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. 1.Facial Facial n.or brachial pluxes injury 2. 2.Skull Skull fractures 3. 3.Heamatoma Heamatoma (caput saccundum) 4. 4.Intracranial Intracranial Hmg - Maternal: 1. 1.Tear Tear and laceration of the cervix 2. 2.Rupture Rupture of bladder 3. 3.Extension Extension of episitomy 4. 4.Bleeding Bleeding 5. 5.Infections Infections
Types:
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simpson
- piper
- Kielland
Indications: Same as forceps.. PLUS few more points ! Prerequities: Prerequities: Full term baby Full flexion of the head Sucon pressure < 600 mmHg Not more than 3 applicaon Don’t twist the cup ! •
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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 spatula (2 ends)
- Endocervical swab
- Fixator
- Slide
Use:
1.Obtain swab form any fluid or discharge 2.High vaginal swab
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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. 1.Rupture Rupture of membrane is a must; spontaneous or artificial 2. 2.Little Little chance of infection; mother & fetus 3. 3.Scalp Scalp trauma Contraindictions: 1. 1.Maternal Maternal infection e.g HIV, herpes simplex 2. 2.Sever Sever fetal coagulopathy
(ovum forcepse) Curved
Stright
Uses: 1. 2.
Remove conceptional product, intrautrine, cervical polyp 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
