Physiology of Reproduction

Human Chorionic Gonadotropin (hCG): placental syncytiotrophoblast, blood 10d after fertilization, peak 9-10w, plateau at 20-22w. Maintains corpus luteum, regulate steroid biosynthesis and stimulate testosterone production in fetal male testes hCG = twin pregnancy, hydatidiform mole, choriocarcinoma, embryonal carcinoma hCG = ectopic pregnancy, threatened abortion, missed abortion Human Placental Lactogen: similar to growth hormone and prolactin, level = placental growth, rising throughout pregnancy Insulin Antagonist and predisposes pregnancy to glucose intolerance and diabetes hPL = threatened abortion, IUGR Progestrone: corpus luteum up to 6-7w, corpus luteum & placenta between 7 & 9w and placenta after 9w Induces endometrial secretary changes for implantation and later induces immune tolerance for pregnancy to prevent contraction. Estrogen: Estradiol: nonpregnant reproductive years, follicle Estriol: pregnancy, placenta from fetal adrenal gland Estrone: after menopause, peripheral adipose tissue

Physiologic Changes in Pregnancy

Skin Striae Gravidarum: stretch marks Spider Angiomata and Palmer Erythema: due to increased skin vascularity Chadwick sign: blue/purplish discoloration of vagina and cervix due to vascularity Linea nigra: increased pigmentation of abdominal midline Cholasma: blotchy pigmentation of nose and face CVS: A systolic ejection murmur along left sternal border is normal in pregnancy. Diastolic Murmur is NEVER normal in pregnancy. Elevated BP is NEVER normal in pregnancy. Arterial Blood Pressure Venous Pressure Peripheral Vascular Resistant CO = HR + SV Systolic Diastolic Central Unchanged femoral = x

Fetal Circulation: fetus has 3 in utero shunts: ductus venosus, foramen ovale and ductus arteriosus. Hematologic: RBC, Plasma, Hb (nadir at 28-30w, physiologic dilution, NOT anemia) Hct, WBC, ESR, unchanged platelet count, coagulating factors VII VIII IX X (leading to hypercoagulability state) GI: gastric-colonic motility and emptying-transit time due to progesterone effect on smooth muscle = constipation Pulmonary: unchanged RR, tidal volume, minute ventilation, residual volume, ABG = respiratory alkalosis (alkalotic urine) Renal: GFR/renal plasma flow/creatinine clearance, serum BUN/creatinine/uric acid, urine glucose, unchanged urine protein Kidney: size and renal blood flow (reverses after 3m postpartum) Ureter: diameter due to progesterone (R>L) Endocrine: Pituitary: size due to vascularity, susceptible to ischemia from postpartum BP (Sheehan Syndrome=hypopituitarism= agalactorrhea) Adrenal gland: Unchanged size but cortisol production Thyroid: size due to vascularity, thyroid bonding globulin, total T3-T4, unchanged free T3-T4

Physiology of Lactation:
Reproductive hormones develop breast in puberty & lactation. Estrogen promotes growth OF ducts, progesterone develops milk producing alveolar cells, prolactin stimulates milk production and oxytocin released in response to sucking causes milk ejection. Expulsion of placenta at delivery initiates milk production and cause drop in circulating estrogen & progesterone. Estrogen antagonizes effect of prolactin on milk production. Colostrum contains more protein, less fat, IgA antibody (passive immunity).

Teratology
Stages of Teratogenesis: nd Conception to end of 2 week: embryo will either survive intact or die Postconception weeks 3-8: greatest teratogenic risk After week 9 of postconcetion: low teratogenicity but diminished organ hypertrophy and hyperplasia

Teratogens
Infectious: chlamydia & gonorrhea cause neonatal eye & ear infection, rubella, CMV, herpes virus, syphilis, (toxoplasmosis) Ionizing radiation: No SINGLE diagnostic procedure threatens the embryo or fetus. No increase in fetal anomalies or pregnancy loses with exposure of <5 rads. Greatest risk between 8-15 weeks of gestation at doses of at least 20 rads. st nd rd Chemotherapy: Risk in 1 trimester only. 2 & 3 trimester fetuses are remarkably resistant to chemotherapeutic agents. Tobacco: IUGR and preterm delivery but NO specific syndrome. Alcohol: fetal alcohol syndrome: IUGR, midfacial hypoplasia, microcephaly, mental retardation, developmental delay, short palpebral fissures, long philtrum, multiple joint anomalies and cardiac defects. Cocaine: placental abruption, preterm delivery, intraventricular hemorrhage & IUGR Marijuana: preterm delivery but NO syndrome Medications: 1-2 % congenital malformations. FDA Catagories of Drugs: A: no risk. Acetaminophen, thyroxine, folic acid and magnesium sulfate B: no risk in humans. Penicillin, cephalosporins, methyldopa, insulin, Pepcid, Reglan, Tagamet, Vistaril, Paxil, Prozac, Benadryl and Dramamine C: risk cannot be ruled out. Codeine, Decadron, methadone, Bactrim, Cipro, AZT, -blockers, Prilosec, heparin, Protamine, Thorazine, Alupent, Robitussin and Sudafed. D: positive evidence of risk, benefits may outweigh risk: Aspirin, Valium, tetracycline, Dilantin, Depakote & Lithium X: Contraindicated in pregnancy: DES, Accutane (isotretinoin), Danocrine, Pravachol (statin), Coumadin and Cafergot. DES Syndrome (Diethylstilbestrol/synthetic estrogen): T-shaped uterus, vaginal adenosis (predisposition to vaginal clear cell carcinoma), cervical hood, incompetent cervix, preterm delivery Isotretinoin (Accutane): Congenital deafness, microtia (congenital deformity of external ear), CNS defects, congenital heart defects Danocrine (steroid): female fetus with clitoral hypertrophy, labial fusion, urogenital sinus defect, vaginal atresia & ambiguous genitalia Warfarin (Coumadin): Chondrodysplasia (stippled epiphysis), microcephaly, mental retardation, optic atrophy Fetal Hydantoin Syndrome (Dilantin/phenytoin): IUGR, craniofacial dysmorphysim (epicanthal folds, depressed nasal bridge, oral clefts), mental retardation, microcephaly, nail hypoplasia, heart defects. Lithium (Ebsteins Anomaly): right heart defect Streptomycin: VIII nerve damage, hearing loss th Tetracycline: deciduous teeth discoloration after 4 month Thalidomide: Phocomelia, limb reduction defects, ear/nasal anomalies, cardiac defects, pyloric or duodenal stenosis Trimethadione: facial dysmorphism (short upturned nose, slanted eyebrows), cardiac defects, IUGR, mental retardation Valporic Acid (Depakote): Neural tube defects (spina bifida), cleft lip, renal defects

Terminology
Gravidity: total number of pregnancies (irrespective of pregnancy duration) Nulligravida: not currently pregnant and never been pregnant Primigravida: currently pregnant for the first time Multigravida: currently pregnant with more than one time Parity: total number of pregnancies achieving 20 weeks of gestation Nullipara: never carried a pregnancy achieving 20 weeks of gestation Primipara: carried one pregnancy achieving 20 weeks of gestation Multipara: carried more than one pregnancy achieving 20 weeks of gestation Parturient: woman in labour Puerpera: woman who has just given birth Abortion: pregnancy loss prior to 20 menstrual weeks Antepartum death: fetal death between 20 menstrual weeks and onset of labor Intrapartum Death: fetal death from onset of labor to birth. Fetal death: fetal death between 20 menstrual weeks and birth Perinatal death: fetal/neonatal death from 20 menstrual weeks to 28 days after birth Neonatal death: newborn death between birth and first 28 days of life Infant death: infant death between birth and first year of life Maternal death: woman who died during pregnancy or within 90 days of birth Birth Rate: live births/1000 total population Fertility rate: live births/1000 women aging 15-45 years Fetal mortality rate: fetal deaths/1000 total births Neonatal Mortality Rate: neonatal deaths/1000 live births Perinatal mortality rate: fetal + neonatal deaths/ 1000 total births Infant mortality rate: infant death/1000 live births Maternal Mortality Rate: maternal death/100,000 live births.

Genetic Disorders
Indications for Genetic Counseling: 1. Advanced maternal age: 35 years at higher risk of trisomy 18 & 21 2. Previous child: neonatal death, mental retardation, aneuploidy, known genetic disorder 3. Pregnancy/fetal losses: stillborn with birth defects, multiple pregnancy/fetal losses 4. Family History: genetic diseases, birth defects, mental retardation 5. Abnormal prenatal tests: triple marker screen, sonogram 6. Parental Aneuploidy Aneuploidy: cells contain an extra or missing chromosome. Most common is trisomy (extra chromosome). Most autosomal trisomies result in spontaneous abortions. The most common trisomy in first trimester losses is trisomy 16 (47 XX+16) and the most common trisomy at term is trisomy 21 (47XX+21). Monosomy is missing of single chromosome for example Monosomy X (45, X). Polyploidy: cells contain complete sets of extra chromosomes. Most common is triploidy with 69 chromosomes (69, XXY), then tetraploidy with 92 chromosomes. Example of triploidy is incomplete molar pregnancy, in which egg is fertilized by two sperms. Chromosomal Deletion: Example is del (5p)/cri du chat syndrome with deletion of short arm of chromosome 5.

Genetics of Pregnancy Loss

50% of 1 T fetal losses are due to abnormal chromosomes. Common aneuploidies in miscarriages are trisomy 16 and monosomy X. Turners Syndrome (45,X) or Gonadal Dysgenesis/ Monosomy X: Mostly loss of paternal X chromosome. 98% result in spontaneous abortion. U/S shows nuchal skin fold thickening & cystic hygroma. Those fetuses that survive at term have absence of secondary sexual development, short stature, streak gonads, primary amenorrhea, primary infertility, broad chest and neck webbing. Urinary anomalies and aortic coarctation is common. Normal intelligence. Klinefelter Syndrome (47, XXY): Diagnosis seldom made before puberty. Low IQ, learning disorders, tall stature, testicular atrophy, azoospermia, gynecomastia and truncal obesity is seen. Down syndrome (47, XX+21) or Trisomy 21: higher incidence with advanced maternal age. Have mental retardation, short stature, muscular hypotonia, brachycephaly and short neck. Facial features are oblique orbital fissure, flat nasal bridge, small ears, nystagmus and protruding tongue. Congenital heart disease (endocardial cushion defects) is more common along with duodenal atresia. Edward Syndrome or Trisomy 18: seen with advanced maternal age. Associated with profound mental retardation, rocker-bottom feet and clenched fists. Survival to age of 1 year is only 40%. Patau syndrome or trisomy 13: seen with advanced maternal age. Associated with profound mental retardation, cyclopia, proboscis, holoprosencephaly, and severe cleft lip with palate. . Survival to age of 1 year is only 40%.
st

Mendelian Genetics
Autosomal Dominant: transmission occurs equally to males and females, and serial generations are affected. Gross anatomic anomalies are the most common findings. Age of onset is delayed, with variability in clinical expression. Each affected individual has an affected parent (unless its a new mutation) and transmit disease to 50% of offspring. Unaffected individuals bear unaffected children. No carrier states. Examples: Polydactyly, Marfan syndrome. Polycystic kidney, Huntington Chorea, Myotonic Dystrophy, Neurofibromatosis, Achondroplasia, Osteogenesis Imperfecta. Autosomal Recessive: transmission occurs equally to males and females, but disease often skips generations. Enzyme deficiencies are most common finding. Age of onset is earlier with consistency in clinical expression. If both parents are heterozygous for the gene, 25% of offspring are affected, 50% are carriers, and 25% are normal. If one parent is homozygous and one is heterozygous, 50% of offspring will be affected and 50% will be carriers. If both parents are homozygous, 100% of children will be affected. Carrier states are common, male & female. Examples: deafness, Albinism, phenylketonuria, Tay-Sachs disease, cystic fibrosis, Sickle cell anemia, Thalassemia, congenital adrenal hyperplasia and Wilson Disease X-linked Recessive: Functionally dominant in men, but may be dominant or recessive in women. No male to male transmission because the father gives only his Y chromosome to his son. Transmission is 100% male to female. The usual transmission is from heterozygous females carriers to male offsprings in an autosomal dominant pattern. The disease is expressed only in all males. Family history shows the disorder only in male relatives, and commonly in maternal uncles. Examples: Hemophilia A, Diabetes Inspidus, G-6-PD deficiency, color blindness, hydrocephalus, Duchenne muscular dystrophy and complete androgen insensitivity. X-linked Dominant: two types: 1. Disease is manifested in female heterozygotes as well as carrier males (hemizygotes). Example: hypophosphatemic rickets. 2. Disease is manifested in female heterozygotes, but is lethal in males. The increased spontaneous abortion rate represents male fetus. Example: incontinentia pigmenti, focal dermal hypoplasia and orofaciodigital syndrome.

Yes

Every Generation? No carrier states?

No

Dominant (Anatomic Disorders) Lethal in males? No Yes Autosomal X-linked Achondroplasia Hypophosphoric Rickets

Recessive (Enzyme Disorders) Father gives it to son? Yes Autosomal CF, TS, SC, PKU, CAH No X-linked Hemophilia

Multifactorial Inheritance
70% of birth defects are multifactorial (genetic & environmental). The more severe the malformation, the higher the risk for recurrence. Neural tube Defect (NTD): failure of neural tube closure by days 26-28 of embryonic life. It ranges from anencephaly to very slight vertebral defects. Anencephaly and spina bifida occur with equal frequency. Polyhydramnios is common. Preconception folic acid intake decreases incidence. Women at high risk should take 4mg of folic acid. All women should take 0.4mg of folic acid. Congenital Heart Disease: majority are multifactorial with recurrence risk of 2%. Preconception folate reduces risk. nd rd Cleft Lip & Palate: Risk of cleft lip in 2 child of unaffected parents is 4%. If two children are affected, risk of 3 child being affected is 10%. Pyloric Stenosis: More common in males. If affected parent is female, the risk of offspring is much greater.

Induced Abortion
Early 1 trimester abortions pose no long term risk. No association between abortion and breast cancer or any other cancer reported. Risk of maternal death associated with abortion increases with advanced gestational age. First-Trimester Methods Vacuum Curettage Dilation & curettage: most common abortion procedure performed before 13w gestation Prophylactic antibiotics, sedation, paracervical block and local anesthesia are applied. Cervical canal is dilated with metal dilators or hygroscopic/osmotic dilators (laminaria). Complications are rare and include endometritis & retained POC (repeat curettage). Medical Abortion: oral mifepristone (Mifeprex, a progesterone antagonist) and oral misoprostol (Cytotec, prostaglandin E1) used only on first 63 days of amenorrhea. 85% will abort within 3d. The earlier the gestational age, the higher the success rate. 2% of patients abort incompletely and require vacuum curettage. Rare cases of Clostridium sordellii sepsis have been reported. Second-Trimester Methods nd Dilation & Evacuation: most common abortion procedure in 2 trimester. Cervical dilation is performed by inserting osmotic laminaria dilators 24h prior to procedure. Cervical dilation in mm should equal number of weeks of gestation (18w=18mm). Pain relief is achieved. 13-14w abortions are performed by vacuum aspiration alone. After 14 w, fetus is morcellated and removed in pieces under U/S guidance. An intact D&E (partial birth abortion) involves more advanced pregnancies, with >2d of laminaria dilation to obtain wide cervical dilation allowing assisted breech delivery of fetus under U/S guidance and decompression of calvaria. Immediate complications are uterine perforation, retained tissue, hemorrhage, infection and rarely DIC. Delayed complications are cervical trauma with resulting cervical insufficiency.
st

Spontaneous Abortion
Definition: Bleeding before 12w gestation. Etiology: chromosomal abnormalities in fetus, Mendelian disorders and rarely Anti-cardiolipin Ab (Antiphospholipid syndrome: women with SLE produce Ab against their own vascular system and fetoplacental tissues. Treatment is subcutaneous Heparin) Clinic: Speculum exam to rule out vaginal/cervical lesions, molar & ectopic pregnancy. RhoGAM to all Rh- gravidas who undergo D&C. Missed Abortion: Sonogram finding of a nonviable pregnancy without vaginal bleeding, uterine cramping or cervical dilation. Management: Scheduled suction D&C/conservative awaiting a spontaneous completed abortion/induce contractions with misoprostol Threatened Abortion: Sonogram finding of a nonviable pregnancy with vaginal bleeding but no cervical dilation. Half will reach term. Management: Observation. No intervention is indicated and effective. Inevitable Abortion: Vaginal bleeding and uterine cramping leading to cervical dilation, but no POC has yet been passed. Management: Emergency suction D&C. Incomplete Abortion: Vaginal bleeding and uterine cramping leading to cervical dilation, with some, but not all POC passed. Management: Emergency suction D&C. Completed Abortion: Vaginal bleeding and uterine cramping have led to passage of all POC, confirmed by sonogram (no debris). Management: Conservative if intrauterine pregnancy was previously confirmed; otherwise, obtain weekly serial -hCG to r/o ectopic pregnancy.

Fetal Demise
Definition: In utero death of fetus after 20w gestation before birth. Antenatal Demise: before labor. Intrapartum Demise: after onset of labor. Complications: DIC (prolonged fetal demise >2w due to release of tissue thromboplastin from deteriorating fetal organs) & grief resolution. Risk Factors: idiopathic, antiphospholipid syndrome, maternal diabetes, maternal trauma, maternal isoimmunization, fetal aneuploidy/infection. Presentation: uterine fundus less than dates (before 20w) and absence of fetal movements (after 20w) Diagnosis: lack of fetal cardiac activity in U/S Lab: Rule out coagulopathy by testing platelet count, d-dimer, fibrinogen, prothrombin time and pTT, Management: DIC present: immediate delivery with selective blood product transfusion No DIC present: Schedule delivery after a number of days to allow an appropriate grief response begins, or if patient wishes conservative management, follow weekly serial DIC lab tests. Mode of delivery: D&E in pregnancies <20w if no fetal autopsy indicated. Induction of labor with vaginal prostaglandin in pregnancies >20w or if a fetal autopsy is indicated. Caesarian delivery is NEVER appropriate for death fetus. Psychosocial issues: allow patient and family to see the fetus, hold the fetus, name the fetus and have a burial. Identify cause: cervical & placental cultures for suspected infection, autopsy for suspected lethal anatomic syndrome, karyotype for suspected aneuploidy, total body x-ray for suspected osteochondrodysplasia, maternal blood for Kleihauer-Betke test (peripheral smear for suspected fetomaternal bleed).

Ectopic Pregnancy
Definition: pregnancy in which implantation has occurred outside uterine cavity. Most common location is distal ampulla of oviduct. DDx: if positive pregnancy test, ddx with threatened abortion, incomplete abortion, ectopic pregnancy & hydatidiform mole. Risk Factors: tubal scarring and adhesions obstructing normal zygote migration to uterine cavity, due to previous PID (most common), IUD, tubal ligation, tubal surgery, congenital (diethylstilbestrol or DES exposure) and idiopathic. Presentation: Unruptured: secondary amenorrhea, vaginal bleeding, unilateral pelvic-abdominal pain and unilateral adnexal & cervical motion tenderness. NO uterine enlargement & fever. Ruptured: above triad, peritoneal irritation & hemodynamically unstable. Lab: Positive -hCG test. U/S may or may not reveal adnexal mass but NO IUP will be seen. Diagnosis: NO intrauterine gestational sac seen with vaginal U/S when serum -hCG titer >1500mIU
Management:

Ruptured ectopic: immediate surgical intervention (Salpingectomy) Intrauterine Pregnancy: if U/S reveals IUP and threatened abortion is diagnosed, put patient at bed rest. if hydatidiform mole is diagnosed, treat with suction curettage & follow up on a weekly basis with -hCG. Possible ectopic: if U/S does not reveal an IUP but -hCG is < 1500mIU, repeat quantitative -hCG and vaginal U/S every 2-3d. Unruptured ectopic: o Methotrexate: pregnancy mass <3.5cm, absence of fetal heart motion, -hCG<6000 mIU, no history of folic supplementation. Follow up with serial -hCG levels to ensure pregnancy resolution. RhoGAM for Rh-negative women. o Laparoscopy: if above criteria for methotrexate are exceeded, surgical evacuation by laparoscopy or laparotomy is

done. Salpingostomy for unruptured ampullary tubal pregnancy, Segmental resection for isthmic tubal pregnancy. Salpingectomy for raptured ectopic pregnancy or those with no desire for further fertility. Follow up with serial hCG levels to ensure pregnancy resolution. RhoGAM for Rh-negative women.

Obstetric Procedure
Obstetric Ultrasound: Transvaginal is used in T1 and transabdominal is used any time. NO adverse effects. Chorionic Villus Sampling (CVS): performed transcervically or transabdominally, between 10-12w, under U/S guidance without anesthesia. Aspirated villi are sent for karyotyping. Fetus and villi have common origin, so their karyotype is 99% identical. Pregnancy loss rate is 0.7%. Amniocentesis: amniotic fluid aspiration is performed after 15w, under U/S guidance and without anesthesia. Fetal karyotyping is performed on Amniocytes (desquamated living fetal cells) and NTD (Neural tube defect) screening is performed on amniotic fluid with biochemical analysis (AFAFP and acetylcholinesterase). Procedure related pregnancy loss rate is 0.5%. Percutaneous Umbilical Blood Sample (PUBS): transabdominal aspiration of fetal blood from umbilical vein after 20w, under U/S guidance. It is diagnostic (blood gases, karyotype, IgG/ IgM antibodies) and therapeutic (intrauterine transfusion with fetal anemia). Pregnancy loss rate is 1-2%. Fetoscopy: Transabdominal procedure performed after 20w in OR under regional or general anesthesia. Used for intrauterine surgery or fetal skin biopsy (for suspected fetal ichthyosis). Laser is used for coagulating placental vessels in twin-twin transfusion syndrome (TTTS). Risks are bleeding, infection, membrane rapture and fetal loss (rate is 2-5%). Cervical Cerclage: transvaginal suturing of cervix between 14-24w, under regional or general anesthesia for cervical insufficiency. Risks include bleeding, chorioamnionitis, infection and membrane rapture. The risks are higher in emergency procedures compared with elective cerclage.

Prenatal Management of Normal Pregnancy Diagnosis of Pregnancy

Presumptive Signs: amenorrhea, breast tenderness, nausea, vomiting, increased skin pigmentation and skin striae. Probable signs: enlargement of uterus, maternal sensation of uterine contractions or fetal movements, Hegar sign (softening of junction between corpus and cervix) and positive urine or serum -hCG testing. Positive Signs: fetal heart tones, sonographic visualization of fetus, perception of fetal movements by examiner and x-ray showing a fetal skeleton.

Establishing Gestational Age

Conception dating: 266 d or 38w post-conception (NOTE: ovulation takes place on day 14 of 4w cycle, day 7 of 3w cycle and day 21 of 5w cycle.) Menstrual Dating: 280d or 40w from LMP (assuming cycle length is 28d). Accuracy of menstrual history is 1w. Naegeles Rule: LMP 3m + 7d = Calculated Due Date Basal Body Temperature: BBT rises due to progesterone. Accuracy of BBT is 1w.

Normal Pregnancy Events

First Trimester: Conception to 13w (assuming 40 menstrual week pregnancy) Normal symptoms are nausea, vomiting, fatigue, breast tenderness and frequent urination. Average weight gain is 5-8 pounds. Spotting and bleeding occur in 20% cases, 50% of which will continue successfully. Complications include spontaneous abortion. Second Trimester: 13-26w Normal symptoms are feeling of well-being, round ligament pain, Braxton-Hicks (painless, low intensity, long duration contractions starting at 14w), Quickening (maternal awareness of fetal movement, at 18-20w primigravidas & 16-20w multigravidas). Weight gain is 1 pound/w after 20w. Complications include incompetent cervix, premature membrane rapture and premature labor. Third Trimester: 26-40w Normal Symptoms are decreased libido, lower back & leg pain, urinary frequency and Braxton Hicks contractions. Lightening is descent of fetal head into pelvis resulting in easier breathing and pelvic pressure. Bloody show describes vaginal passage of bloody endocervical mucus due to cervical dilation before labor. Average weight gain is 1 pound/w after 20w. Complications include premature membrane rapture, premature labor, preeclampsia, UTI, anemia and gestational diabetes.

Complaints
Backache Bleeding Gums Breast Enlargement Carpal Tunnel Skin Changes Dizziness Fatigue Fluid Retention Hair shedding Headache Leg cramps Morning sickness Nosebleeds Stretch Marks Stress Incontinence Varicose Vein

Cause
Change in center of gravity Increased blood flow to gums. Bleeding + swelling = epulis 400g each (1-2 cup sizes) Numbness, tingling, burning or pain in 2-3 digits supplied by median nerve Cholasma(brown patches on face), linea nigra, hyperpigmentation of nipple Low BP results in postural hypertension rapid hormonal changes steroid & serum albumin. Edema is NOT criterion for preeclampsia. in pregnancy. Telogen effluvium (excessive shedding) at 1-5m after birth Increased estrogen levels Elevated -hCG Vasodilation and increased vascular supply Striae gravidarum: genetic predisposition, associated with risk of lacerations Enlarged uterus puts pressure on bladder Increased blood volume, progesterone, lower extremity venous pressure

Management
Correct posture conservative Support bra Wrist splint conservative Avoid rapid standing Adequate resting Elevating legs, support hose conservative Physical therapy, drugs at last Stretching, hydration, Ca tablets Eat small meals (carbohydrates) Saline drops, avoid nasal sprays conservative Kegal Excercises Avoid prolong standing & sitting

Pregnancy Danger Signs Vaginal Bleeding Vaginal Fluid Leakage Epigastric Pain Uterine Cramping fetal movements Persistent vomiting Headache, visual changes Pain with urination Chills & fever

Possible Diagnosis Early (spontaneous abortion), Late (abruption, pravia) Rupture of Membrane, urinary Incontinence Severe preeclampsia Preterm Labor, Preterm contractions Fetal compromise Hyperemesis (early), hepatitis, pyelonephritis Severe preeclampsia Cystitis, pyelonephritis Chorioamnionitis, pyelonephritis

Immunization Safe: antigens from killed or inactivated organisms: Influenza: all pregnant women in flu season Hepatitis A & B: pre- and post-exposure Pneumococcus: only high risk women Meningococcus: in unusual outbreaks Typhoid: not routinely recommended Unsafe: antigens from live attenuated organisms: Measles, Mumps, Rubella, Polio, yellow fever, Varicella

First Trimester Lab Tests

Complete Blood Count Hb & Hct: Normal female Hb is 12-14g/dL and normal pregnancy Hb is 10-12g/dL. Low Hb and Hct reflect normal dilution. MCV: Hb + MCV (<80m3)= iron deficiency anemia/thalassemia Hb + MCV (>100) = folate deficiency Platelet Count: <150,000/mm3 indicates idiopathic thrombocytopenic purpura or pregnancy induced thrombocytopenia. DIC is rare. Leukocyte Count: normally upto 16000/mm3 in pregnancy. Leukopenia suggests immune suppression or leukemia Rubella IgG Antibody: presence rules out primary infection during pregnancy. Absence of Ab leaves the woman at risk for primary infection that can have adverse effects on fetus, especially in T1. Rubella vaccine is contraindicated in pregnancy but is recommended after delivery. HBV: HBsAb indicates successful vaccination. HBsAg represents either a previous or current infection with high risk for vertical transmission of HBV. HBeAg indicates a highly infectious state. Type, Rh, Antibody Screen: blood type & Rh is determined by direct Coombs test. Rh negative patient is at risk for anti-D isoimmunization. Presence of atypical RBC Ab is determined by Indirect Coombs test. If present, it indicates isoimmunization. Follow up tests done for fetus at risk. Cervical Pap Smear: to identify if mother has cervical dysplasia or malignancy. STD Screening Chlamydia and Gonorrhea: Cervical Cultures will identify if fetus is at risk from delivery through an infected birth canal. Syphilis: Screening tests (VDRL/RPR) performed on all pregnant women. Positive tests are followed up with treponema-specific tests (MHA-TP/ FTA) HIV: HIV screening is recommended for all pregnant women, but requires a specific consent. ELISA test detects HIV Ab which is positive only 3m after HIV infection. (All babies born to HIV-positive mothers will be HIV Ab positive.) Western blot test detects presence of HIV core & envelope Ag. Urine Screening Urinalysis: assessment of proteinuria, ketones, glucose, leukocytes & bacteria to screen for underlying renal disease, diabetes and infection. Culture: for asymptomatic bacteriuria (ASB), if left untreated, 30% will progress to pyelonephritis which is associated with septic shock, PE & ARDS. TB Screening: NOT done routinely but only on high risk patients. PPD or Tine test to determines previous exposure to TB. If positive (induration), a chest X-ray is performed to rule out active disease. If chest x-ay is negative, isoniazid (INH) & vit B6 is given for 9m. If chest x-ray is positive, induced sputum is cultured and triple (INH, Rifampin, Ethambutol) begun until cultures define the organisms involved. AntiTB drugs are NOT contraindicated in pregnancy. NO Pyrazinamide or streptomycin in pregnancy

Second Trimester Lab Tests

Maternal Serum - Fetoprotein (MS-AFP): AFP peaks at 12w in fetal serum/amniotic fluid and peaks at 30w in maternal serum. Increased levels seen in open neural tube defect, ventral wall defect, twin pregnancy, placental bleeding, fetal renal disease and sacrococcygeal teratoma. MS-AFP is part of multiple marker screening performed between 15-20w and reported in multiples of median. MS-AFP (>2.5MoM): if , obtain U/S to confirm gestational age. If true gestational age > assumed, it explains the high value. In cases of dating error, repeat MS-AFP if pregnancy is still within 15-20w window. A normal MS-AFP is reassuring. If dates are correct and no explanation is seen on U/S, perform amniocentesis for AF-AFP determination and acetylcholinesterase activity. AF-acetylcholinesterase activity is specific to open NTD. With unexplained MS-AFP but normal AF-AFP, pregnancy is at risk for IUGR, stillbirth and preeclampsia. MS-AFP (<0.85MoM): if dates are correct and no explanation seen on U/S, perform amniocentesis for karyotype. The sensitivity of MSAFP alone for trisomy 21 is only 20%. Note: Normal=1 MoM, Trisomy 21 = 0.75MoM, ONTD = 3.8MoM, Anencephaly = 7.7MoM Triple Marker Screen: measures maternal serum for MS-AFP, -hCG and estriol. Performed at 15-20w and its values are gestational age specific. MS-AFP + estriol +-hCG = Trisomy 21/Down Syndrome. all 3 = Trisomy 18/Edward Syndrome. Perform amniocentesis for karyotyping. Quadruple Marker Screen: Above 3 + Inhibin A. Increases trisomy 21 detection rate to 80%.

Third Trimester Lab Tests

Diabetic Testing Oral Glucose Tolerance Test (OGTT): This is a screening test done in all pregnant women between 24-28w. No fasting is needed. A 50g glucose load is given and serum glucose is measured 1h later. Normal value is < 140mg/dl. If 140mg/dL then 3h 100g OGTT is done. 3h 100g OGTT: this is a definitive test for glucose tolerance in pregnancy. After an overnight fast, FBS is tested, an FBS> 125mg/dL indicates over diabetes mellitus, and no further testing is performed. If FBS < 126mg/dL, administer a 100g glucose load, followed by glucose levels at 1,2 and 3h. Normal values are FBS < 95mg/dL, 1h <180mg/dL, 2h <155 mg/dL and 3h <140 mg/dL. Gestational diabetes is diagnosed if two or more values are abnormal. Impaired glucose intolerance is diagnosed if only one value is abnormal. Complete Blood Count Anemia: CBC should be performed between 24-28w gestation in all women. With increasing diversion of iron to fetus in T2 and T3, iron deficiency which was not present early in pregnancy may develop, especially in women who are not taking iron supplementation. A Hb <10g/dL = anemia Platelet Count: reassessment of pregnancy-induced thrombocytopenia Atypical Antibody Screen: Before giving prophylactic RhoGAM to an Rh-negative woman, an indirect Coombs test is done at 28w to ensure she has not become isoimmunized since her previous negative AAT earlier in pregnancy. 2% Rh-negative women becomes isoimmunized from spontaneous feto-maternal bleeding before 28w. If she already has anti-D antibodies, administration of RhoGAM is futile.

Perinatal Infections
Group B -Hemolytic Streptococci (GBS):
Normal GI tract flora. 30% women have asymptomatic vaginal colonization with GBS. Most neonates born to colonized mothers are culture positive Fetal Infection: pneumonia and newborn sepsis within few hours to days of birth is common. Meningitis after first week of life is rare. Prevention: Intrapartum antibiotic prophylaxis (IV penicillin G. If penicillin allergic, use clindamycin or erythromycin) in following: No screening: positive GBS urine culture or a previous baby with GBS sepsis. Screening by vaginal culture: positive T3 vaginal cultures done at 36-37w Intrapartum risk factors: Preterm gestation, membrane ruptured >18h or maternal fever. No vaginal cultures are obtained.

Toxoplasmosis:
Toxoplasma gondii is transmitted from exposure to infected cats feces, drinking raw goat milk or eating raw meat. Vertical infection is only possible during parasitemia of primary infection because result is lifelong immunity. 40% of pregnant women are toxoplasmosis IgG seropositive. T1 infection risk is low but infections are most serious, even lethal. T3 infection risk is high but infections are mostly asymptomatic. Fetal Infection: symmetrical IUGR, nonimmune fetal hydrops, microcephaly, intracranial calcification Neonatal Findings: chorioretinitis, seizures, hepatosplenomegaly and thrombocytopenia. Prevention: Avoid infected cats feces, drinking raw goat milk or eating raw meat Treatment: Pyrimethamine and sulfadiazine to treat known infection. Spiramycin to prevent vertical transmission to fetus.

Varicella:
Varicella is a DNA virus spreading by respiratory droplets causing chicken pox and herpes zoster. 90% women are immune by adulthood. Fetal Infection: transplacental infection rate is 25-40%. Neonatal Finding: Congenital varicella syndrome is characterized by zigzag skin lesions, microphthalmia, cataracts, chorioretinitis, extremity hypoplasia and motor & sensory defects. The greatest neonatal risk is if maternal rash appears between 5d antepartum and 2d postpartum. Maternal Infection: 10% women will develop varicella pneumonia with high maternal morbidity and mortality. Communicability begins 1-2d before vesicles appear and lasts until all vesicles are crushed over. Pruritic vesicles begin on head & neck, progressing to trunk. Infection can trigger labor. Prevention: Administer VZIG (varicella zoster immune globulin) to a susceptible gravida within 96h of exposure. Live-attenuated varicella virus (Varivax III) can be administered to nonpregnant or postpartum to varicella IgG-Ab-negative women. Treatment: IV Acyclovir for varicella pneumonia, encephalitis or the immunocompromised.

Rubella: A highly contagious RNA virus spreading by respiratory droplets. 85% pregnant women are rubella IgG seropositive. Vertical transmission
is only possible during viremia of a primary infection because the result is lifelong immunity. Fetal Infection: transplacental infection rate is >90% in first 10w of pregnancy but 5% in T3. Manifests as symmetrical IUGR, microcephaly or VSD. Neonatal Findings: Congenital Rubella Syndrome is characterized by congenital deafness, congenital heart disease, congenital cataract, mental retardation, hepatosplenomegaly, thrombocytopenia and blueberry muffin rash. Prevention: All pregnant women should undergo rubella IgG Ab screening. Rubella susceptible women should avoid known rubella cases, then receive active immunization after delivery. Since rubella vaccine is live attenuated virus, pregnancy should be avoided for 1m after immunization. Treatment: No specific treatment

Cytomegalovirus (CMV): DNA herpes virus spreading by infected body secretions. 50% women are CVM IgG seropositive. Vertical transmission is
only possible during viremia of primary infection, however, because result is lifelong latency, fetal infection can occur with reactivation. Fetal Infection: transplacental infection rate is 50% in all trimesters, but <1% with recurrent infection. Manifests as symmetrical IUGR, nonimmune fetal hydrops, microcephaly, cerebral calcification in a periventricular distribution. Neonatal Finding: Congenital CMV syndrome is common congenital viral syndrome and common cause of sensineural deafness in children. Only 10% of infected infants show petechiae, meningoencephalitis, periventricular calcification, hepatosplenomegaly, thrombocytopenia and jaundice. Maternal Infection: CMV infection during pregnancy is mild, low-morbidity condition appearing as mononucleosis-like syndrome with hepatitis. Prevention: Follow precautions with all body fluids. Avoid transfusion with CMV-positive blood. Treatment: ganciclovir.

Herpes Simplex Virus (HSV): A DNA virus that spreads by intimate mucocutaneous contact. 50% are HSV IgG seropositive. Most genital herpes
result from HSV II. Transplacental transmission is only possible during viremia of primary infection but is rare. HSV infection predisposes to lifelong latency with periodic recurrent attacks. Common route of fetal infection is contact with maternal genital lesions during a recurrent HSP episode. Fetal Infection: transplacental infection rate is 50%. Manifests with symmetrical IUGR, microcephaly and cerebral calcification. Neonatal Finding: with passage through HSV-infected birth canal, neonatal attack rate is 50% with primary infection, <5% with recurrent infection. Neonatal mortality rate is 50%. Survivals have petechiae, meningoencephalitis, mental retardation, pneumonia, hepatosplenomegaly & jaundice. Maternal infection: Primary herpes results from viremia with fever, malaise, adenopathy & diffuse genital lesion (vaginal, cervix, vulva & urethra). Transplacental fetal infection is possible. Recurrent herpes results from migration of virus from dorsal root ganglion but is localized and less severe with no systemic manifestations. Fetal infection results only from passing through a birth canal with lesions present. Prevention: Cesarean section is performed in presence of genital HSV lesions at the time of labor. If membranes are raptured>8-12h, the virus may already have infected the fetus and cesarean delivery would be of no value. Treatment: Acyclovir

HIV: Transplacental infection occurs, but major route of transmission is contact with infected genital secretions at time of vaginal delivery.
Fetal Infection: vertical transmission rate is 30% without maternal azidothymidine (AZT) prophylaxis, 10% with AZT and vaginal delivery, 1% with AZT & cesarean delivery. With elective cesarean section without labor and before membrane rupture, the perinatal infection rate may be <5%. Neonatal Finding: At birth neonates of HIV-positive women will have positive HIV tests from transplacental passive IgG passage. HIV-infected breast milk can potentially transmit the disease to newborn. Progression from HIV to AIDS in infants is more rapid than adults. Maternal Infection: Pregnancy in HIV-positive woman does not enhance progression to AIDS Prevention: infected pregnant women should take triple-drug therapy including ZDV starting at 14w and continuing throughout pregnancy, Intrapartum and after delivery. Vaginal delivery guidelines are follows: Avoid amniotomy as long as possible. Do not use scalp electrodes in labor Avoid forceps or vacuum extractor operative delivery Use gentle neonatal resuscitation Breast feeding should be avoided in HIV-positive women. Treatment: women with low CD4 counts and high RNA viral loads should receive triple drug therapy starting at 14w to delivery.

Syphilis: Syphilis is caused by Treponema pallidum and does not result in immunity and latency. Transmits by intimate contact between moist
mucous membranes or congenitally through placenta to fetus from an infected mother. Transplacental infection rate is 60% with primary and secondary syphilis but lower with latent or tertiary syphilis. Fetal Infection: Without treatment, early congenital syphilis manifests as nonimmune hydrops, macerated skin, anemia, thrombocytopenia and hepatosplenomegaly. Fetal death rate is high with perinatal mortality rate of 50%. Placenta is typically large and edematous. th Neonatal Findings: late congenital syphilis is diagnosed after 2y of age: Hutchinson teeth, mulberry molars, saber shins, saddle nose, 8 nerve deafness Maternal infection: Primary Syphilis: first stage after infection with chancers that appear 2-3w after contact, commonly the vulva, vagina or cervix. Darkfield microscopy is positive for spirochete but VDRL or RPR test are negative. Chancer disappears spontaneously without treatment. Secondary syphilis: characterized by systemic spirochetemia. 2-3m after contact, fever, malaise, general adenopathy and money spots are seen. Condyloma lata appear on vulva. These also disappear spontaneously without treatment. Darkfield microscopy of condyloma exudate, VDRL and RPR are positive, but diagnosis must be confirmed by treponema-specific test such as FTA-ABS or MHA-TP. Latent Syphilis: absence of symptoms or physical findings. All tests remain positive. 1/3 cases proceed to tertiary state Tertiary syphilis: gummas in CVS (aortitis, saccular aneurysm), CNS (meningitis, tabes dorsalis, dementia, ataxia) or bone (ostitis). Not only the blood tests will be positive but also the CSF will be positive with CNS involvement. Prevention: Vaginal delivery is appropriate, with cesarean section only for obstetric indications. Use of barrier contraceptives should be promoted. Treatment: Single dose of Benzathine penicillin 2.4 million units IM is given in pregnancy. Other antibiotics do not cross the placenta well. Even if the gravida is penicillin allergic, she should still be given a full penicillin dose using an oral desensitization regimen under controlled conditions.

Hepatitis B (HBV): Vertical transmission rate is 40% of all chronic HBV infections. Most HBV infections are asymptomatic.
Fetal Infection: Transplacental infection is rare, occurring mostly in T3. Fetal or neonatal infection arises from exposure to or ingestion of infected genital secretions at the time of vaginal delivery. NO perinatal transmission risk if mother is HBsAb-positive and HBsAg-negative. Neonatal Infection: Neonatal HBV seen in 10% of HBsAg + mothers & 80% in HBsAg+ & HBeAg + both. 80% neonates develop chronic hepatitis. Maternal Infection: Asymptomatic HBV: no impact on maternal health. All pregnant women are screened for HBsAg. if positive, complete hepatitis panel and liver enzymes will be tested. Acute hepatitis: results in RUQ pain and lethargy with billirubin and liver enzymes. Majority will recover normal liver function. Chronic hepatitis: cirrhosis and hepatocellular carcinoma are serious consequences. Prevention: Vaginal delivery is indicated with cesarean section only for obstetric indications. Avoid scalp electrodes in labor and scalp needles in nursery. Neonates of HBsAg positive mothers should receive HBIg and hepatitis B vaccine and breast feeding is acceptable after immunization. HBsAg-negative mothers at high risk should receive HBIg. Active immunization with hepatitis B vaccine is safe in pregnancy. Treatment: No specific therapy for acute hepatitis. Interferon or lamivudine for chronic hepatitis.

Intrauterine Growth Restriction (IUGR): fetus with EFW <5-10th percentile for gestational age OR Birth Weight <2500g (5lb, 8oz).
Dating: An early U/S (<20w) is most accurate if conception date is unknown. Dont change gestational age based on a late sonogram. Fetal Causes: aneuploidy (T21, T18, T13), infection (TORCH), structural anomalies (congenital heart disease, NTD, ventral wall defects) = symmetric Placental Causes: infarction, abruption, twin-twin transfusion syndrome, velamentous cord insertion = asymmetric IUGR Maternal Causes: HTN, small vessel disease (SLE, long standing type 1 diabetes), malnutrition, tobacco, alcohol, street drugs = asymmetric IUGR Symmetrical IUGR: All U/S parameters (HC, BPD, AC, FL) are smaller than expected. Etiology is decreased growth potential. Detailed U/S, karyotype and screening for infection is done. Antepartum tests are usually normal. Asymmetrical IUGR: U/S parameters show head sparing, but abdomen is small. Etiology is placental perfusion. Amniotic Fluid Index is often . Monitoring is with serial U/S, non-stress test, AFI, biophysical profile and umbilical artery Dopplers. Bed rest with lateral recumbent position.

Macrosomia: fetal with estimated fetal weight (EFW) >90-95th percentile for gestational age OR >4000-4500g (8lb,13oz to 9lb, 15oz)
Sonogram EFW: Accuracy in estimating birth weight is poor. Errors in prediction of EFW at term are 400g Risk Factors: Gestational diabetes mellitus, overt diabetes, prolonged gestation, obesity, pregnancy weight gain, multiparity, male fetus. Maternal Hazards: Operative vaginal delivery, perineal laceration, postpartum hemorrhage, emergency C-section, pelvic floor injury. Fetal & Neonatal Hazards: Shoulder dystocia, birth injury and asphyxia, neonatal intensive care admission, hypoglycemia, Erb palsy Management: Elective Cesarean if EFW> 4500g in diabetic mother or >5000g in nondiabetic mother OR early induction (but mostly fails)

Late Pregnancy Bleeding (bleeding after 20w)

Etiology: Cervical (erosions, polyps, rarely carcinoma), vaginal (varicosities, laceration), placental (abruption placenta, placenta previa, vasa previa) Initial Investigation: CBC, DIC workup (platelets, PT, pTT, fibrinogen, D-dimer), type & cross match and sonogram for placental location. NEVER perform a digital or speculum examination until ultrasound study rules out placenta previa. Initial Management: Start an IV line. If maternal vital signs are unstable, run isotonic fluids without dextrose & place urinary catheter to monitor output. If fetal jeopardy is present or gestational age 36w, the goal is delivery.

Abruptio Placenta: A normally implanted placenta separates (partial or complete) from uterine wall before delivery of fetus. Mostly bleeding
is overt and external. If bleeding remains concealed or internal,???? Risk Factors: previous abruption, HTN, maternal trauma, cocaine abuse and premature membrane rupture. Presentation: Mild: minimal bleeding, localized uterine pain & tenderness, no fetal monitor abnormality, incomplete relaxation between contractions Moderate: 25-50% placental separation. Moderate painful bleeding, gradual or abrupt onset, fetal monitoring shows tachycardia, decreased variability or mild late deceleration Severe: >50% placental separation. Abrupt bleeding with continuous knifelike uterine pain, fetal monitoring shows severe late deceleration, bradycardia or even fetal death. Severe DIC may occur. No bleeding (retroplacental hematoma) resulting in increase in fundal height over time and U/S may show retroplacental hematoma. Diagnosis: painful late-trimester vaginal bleeding with normal fundal or lateral uterine wall placental implantation not over lower uterine segment Management: Emergency Cesarean Delivery: if maternal or fetal jeopardy is present as soon as mother is stabilized. NO Cesarean if fetus is dead. Vaginal Delivery: if bleeding is heavy but controlled OR pregnancy >36w. Perform amniotomy and induce labor. Place external monitors. Conservative in-hospital observation: If mother & fetus are stable, remote from term, bleeding is minimal & decreasing and contractions are subsiding. Confirm normal placental implantation with sonogram and replace blood loss with crystalloid and blood products. Complications: hemorrhagic shock with acute tubular necrosis from profound hypotension and DIC from release of tissue thromboplastin. Couvelaire uterus refers to blood extravasating between myometrial fibers, appearing like bruises on serosal surface.

Placenta Previa: Implantation of placenta in lower uterine segment, causing spotting (NO bleeding) early in pregnancy. Usually lower implanted
placenta atrophies and upper placenta hypertrophies resulting in migration of placenta. At term only 0.5% present. Symptomatic placenta previa occurs when painless vaginal bleeding develops due to stretching of lower uterine segment and avulsion of placenta later in pregnancy. Risk Factors: previous placenta previa, multiple gestations, multiparty and advanced maternal age. Presentation: painless late pregnancy bleeding occurring suddenly during rest or activity without warning. It may be preceded by trauma, coitus or pelvic examination. Uterus is nontender and nonirritable.

 Total/complete/central previa: placenta completely covers internal cervical os. MOST DANGEROUS LOCATION Partial previa: placenta partialy covers internal os Marginal/low-lying previa: placental edge is near but not over internal os. Diagnosis: painless late-trimester vaginal bleeding with U/S showing placental implantation over lower uterine segment. Management: NO VAGINAL EXAM Emergency Cesarean Delivery: if maternal or fetal jeopardy is present as soon as mother is stabilized. Conservative in-hospital observation: If mother & fetus are stable and remote from term. Initial bleeding is rarely severe. Complete bed rest. Confirm abnormal placental implantation with sonogram and replace blood loss with crystalloid and blood products. If early in pregnancy, give tocolytic agents. If between 24-34w, give 2 doses of 12mg IM Betametasone separated by 24h to help fetal lung maturity. Vaginal Delivery: if marginal implantation (lower placental edge is >2cm from internal os) and cephalic presentation. Amniotomy (artificial rupture of membrane), no oxytocin and use vacuum extractor. Scheduled Cesarean Delivery: at 36w, if mother is stable and fetal lung maturity confirmed by amniocentesis Complications: Profound hypotension can cause anterior pituitary necrosis (Sheehan Syndrome) or acute tubular necrosis. If placenta previa occurs over a previous uterine scar, the villi may invade into deeper layers, resulting in intractable bleeding requiring Cesarean hysterectomy. Placenta accrete: villi invade deeper layers of endometrial deciduous basalis, but do not penetrate myometrium. 75% Placenta increta: villi invade myometrium, but do not reach uterine serosal surface or bladder. 15% Placenta percreta: villi invade all the way to uterine serosa or into bladder. 5%

Vasa Previa:Rupture of fetal vessels traversing fetal membranes over internal os,causing fetoplacental circulation bleeding &fetal exsanguination
Risk Factors: velamentous insertion of umbilical cord, accessory placental lobes and multiple gestations. Presentation: rupture of membranes and painless vaginal bleeding followed by fetal bradycardia. Diagnosis: Rarely confirmed before delivery but may be suspected when antenatal color Doppler U/S reveals vessel crossing membranes over internal cervical os. Diagnosis is usually confirmed after delivery on examination of placenta and fetal membranes. Management: Immediate Cesarean delivery is essential or the fetus will die from hypovolemia.

Uterine Rupture: Complete separation of pregnant uterus wall with/without expulsion of fetus that endangers life of mother, or fetus, or both.
RF: previous uterine incision (vertical fundal>low segment), myomectomy, excessive oxytocin stimulation, multiparity, marked uterine distension Presentation: vaginal bleeding or bloody urine, abdominal pain & tenderness, increased sudden cessation of uterine contraction with tearin g sensation, loss of station of fetal head and loss of electronic fetal heart rate signal. Followed by hemorrhagic shock and hemiperitonium. Diagnosis: surgical exploration of uterus and identifying the scar. (Rapture mostly occurs during labor, except caesarean scar which raptures in T3 .) Management: Immediate Cesarean Section with uterine repair in stable young women to conserve fertility. Hysterectomy in unstable patients or those who do not desire further childbearing.

Obstetric Complications
Cervical Insufficiency: Inability of uterine cervix to retain a pregnancy to viability in absence of contractions or labor.
Etiology: trauma from rapid forceful cervical dilation associated with T2 abortion procedures, cervical laceration from rapid delivery, injury from deep cervical conization or congenital weakness from diethylstilbestrol (DES) exposure. Diagnosis: Painless cervical dilation between 18-22w with expulsion of a previable living fetus. Management: Elective cerclage placement at 13-16w is appropriate after sonographic demonstration for fetal normality. Emergency cerclage may be considered with sonographic evidence of cervical insufficiency after ruling out labor and Chorioamnionitis. Cerclage removal should take place at 36-37w, after fetal lung maturity has taken place but before usual onset of spontaneous labor that could result in avulsion of suture. McDonald cerclage: places a removable suture in cervix. Benefit is that vaginal delivery can be allowed to take place, avoiding cesarean. Shirodkar cerclage: uses submucosal placement of suture beneath mucosa and left in place. Cesarean delivery is performed at term.

Multiple Gestations: Pregnancy with more than one fetus. Fetuses arise from 1 or more zygotes & are usually separate, but may be conjoined.
Risk Factors: Dizygotic multiple gestations are common. Identifiable risk factors are race, geography, family history or ovulation induction. Risk of twining is 10% with clomiphene citrate & 30% with human menopausal gonadotropin. Monozygotic multiple gestation has no identifiable risks. Clinical Findings: Hyperemesis gravidarum due to high levels of -hCG, large uterus than dates and high levels of maternal serum -fetoprotein. Diagnosis: U/S demonstration of more than one intrauterine fetus. Complications: nutritional anemia (Iron/Folate), preeclampsia, preterm labor, malpresentation, cesarean section & postpartum hemorrhage in all. Dizygotic twins: arise from multiple ovulations with two zygotes, with 2 placenta and 2 amniotic sacs. Monozygotic Twins: arise from one zygote. Chorionicity and amnionicity vary according to duration of time from fertilization to cleavage: Di-Di twins (upto 72h): 2 placentas, 2 amniotic sacs. It has lowest risk. Mono-Di Twins (4-8d): 1 placenta, 2 sacs. Additional complication is twin-twin transfusion. Twins share placenta unequally. The donor twin gets less blood resulting in growth restriction, oligohydramnios and anemia. The recipient twin gets more blood resulting in excessive growth, polyhydramnios and polycythemia. Neonatal course is often complicated. Mono-Mono twins (9-12d): 1 placenta, 1 sac. Additional risks are twin-twin transfusion but particularly umbilical cord entanglement. This is the highest risk of all monozygotic twins. Conjoined Twins (after 12d): Mostly its a lethal condition. Management: Antepartum: iron & folate supplementation, monitor BP, educate about preterm labor symptoms, serial U/S looking for twin-twin transfusion st st nd Intrapartum: vaginal delivery if both are cephalic presentation, cesarean if 1 twin is noncephalic, controversial if 1 is cephalic & 2 noncephalic. Postpartum: Watch for postpartum hemorrhage from uterine atony owing to over-distended uterus.

Isoimmunization: A pregnant woman developing Antibody to foreign RBCs, commonly against those of her current/previous fetuses.
Most common RBC Ag are of Rh system (C, c, D, E, e) with most common being big D. Ab to RBC are detected by indirect Coombs test (AAT). Hemolytic disease of newborn (HDN) is a continuum ranging from hyperbilirubinemia to erythroblastosis fetalis. HDN is caused by maternal Ab crossing into fetal circulation and targeting Ag+ fetal RBCs, resulting in hemolysis. When severe it results in anemia, fetal hydrops and even death. Risk Factors: Mostly occurs when fetal RBCs enter mothers circulation transplacentally at delivery. It also occurs if a woman is transfused with mismatched RBCs. Other risk factors are amniocenthesis, ectopic pregnancy, D&C, abruptio placenta and placenta previa. Protective Factors: ABO incompatibility decreases risk of maternal isoimmunization from foreign RBCs. Naturally occurring anti-A and anti-B antibodies rapidly lyse foreign RBCs before maternal lymphocytes are stimulated to produce active antibodies. Requirements: all must be present. Mother must be Ag Fetus must be Ag+, which means father of pregnancy must also be Ag+ Adequate fetal RBCs must cross over into maternal circulation to stimulate her lymphocytes to produce antibodies to fetal RBC Ag Antibodies must be associated with HDN A significant titer of maternal Ab must be present to cross over into fetal circulation and lead to fetal RBC hemolysis Management: Fetal blood typing by amniocentesis or percutaneous umbilical blood sampling (PUBS). If fetus is RBC Ag-, there is no fetal risk. 1. Determine fetal risk: Fetal risk is present only if: o atypical Antibody are detected in mothers circulation o antibodies are associated with HDN o Ab are 1:8 titer o Father of baby (FOB) is RBC Ag+ No fetal risk is present if: o AAT is negative o Ab are present but not associated with HDN o Ab titer < 1:8 o FOB is RBC Ag If atypical antibody titer is < 1:8, management is conservative. Repeat titer monthly, as long as it remains < 1:8 2. Assess degree of fetal anemia by serial amniocentesis, PUBS or Doppler U/S: if fetus is RBC Ag+ or if fetal blood typing is impossible. Amniotic fluid bilirubin indirectly indicates fetal hemolysis. The bilirubin is plotted on a Liley graph. PUBS directly measure fetal Hct and degree of anemia. Doppler U/S measures peak flow velocity of blood through fetal middle cerebral artery (MCA). fetal anemia worsen, peak flow velocity 3. Intervene if severe anemia. This is diagnosed when amniotic fluid bilirubin is in Liley zone III or PUBS shows fetal Hct 25% or MCA flow is Intrauterine intravascular transfusion is performed if gestational age is <34w. Delivery is performed if gestational age is 34w Prevention: RhoGAM is pooled anti-D IgG passive antibodies given IM to pregnant woman with risk of fetal RBSs passing into her circulation. Passive IgG Ab attacks foreign RBC Ag, causing lysis to occur before maternal lymphocytes become stimulated. RhoGAM is routinely given to RhDmothers at 28w and within 72h of chorionic villus sampling (CVS), amniocentesis, D&C or delivery of RhD+ infant. 300 microgram RhoGAM will neutralize 15ml of fetal RBC or 30ml of fetal whole blood. Kleihauer-Betke test quantitates volume of fetal RBCs in maternal circulation by differential staining of fetal and maternal RBCs on peripheral smear. This assesses if >1 vial needs to be given when large volumes of fetal-maternal bleed may occur (e.g., abruptio placenta)

Preterm Labor
Pregnancy at 20-36w with 3 contractions in 30min and cervical dilation of 2cm or changing Risk Factors: multiple pregnancy, uterine anomalies, PROM and previous preterm labor are common. Other risks are pyelonephritis, Chorioamnionitis, maternal smoking, heavy physical labor, polyhydroamnios, abdominal-pelvic surgery, periodontal disease, bacterial vaginosis, trichomonas vaginalis and ultrasound cervical length < 25mm. Symptoms: Lower abdominal pain or pressure, lower back pain, increased vaginal discharge or bloody show. Particularly in primigravidas, symptoms may be present from hours to days but are not recognized as contractions by the patient. DDx: Preterm contraction: pregnancy at 20-36w with 3 contractions in 30 min and cervical dilation of <2cm and no change. Tocolytic Agents: Parenteral agents may prolong pregnancy but no more than 72h. It provides time to administer maternal IM betamethasone to enhance fetal lung surfactant and transfer mother to a facility with NICU. Oral tocolytic agents are no more effective than placebo. Magnesium Sulfate: it is a competitive inhibitor of Ca. Side effects are muscle weakness, respiratory depression & pulmonary edema. Mg overdose is treated with IV Ca Gluconate. Contraindications are renal insufficiency and myasthenia gravis. -Adrenergic agonists (terbutaline): Side effects are hypotension, tachycardia, hyperglycemia, hypoK and pulmonary edema. Contraindications are cardiac disease, diabetes mellitus and uncontrolled hyperthyroidism. Calcium-channel blockers (Nifedipine): side effects are hypotension, tachycardia and myocardial depression. Contraindication is low BP Prostaglandin synthetase inhibitors (indomethacin): side effects are oligohydramnios, in utero ductus arteriosus closure and neonatal necrotizing enterocolitis. Contraindications are gestational age > 32w. Tocolytic Contraindications: Stopping labor is either dangerous for mother and baby or futile 1. Obstetric: severe abruptio placenta, ruptured membranes, Chorioamnionitis 2. Fetal: lethal anomaly (anencephaly, renal agenesis), fetal demise or jeopardy (repetitive late deceleration) 3. Maternal: eclampsia, severe preeclampsia, advanced cervical dilation

Management: Confirm labor using definition Rule out contraindications to tocolysis using criteria above Initiate IV hydration with isotonic fluids. Start Magnesium sulfate with 5g IV for 20min, then 2g/h Obtain cervical and uterine cultures before giving IV penicillin G (or erythromycin) for group B Streptococcus sepsis prophylaxis Administer maternal IM betamethasone to stimulate fetal type II pneumocyte surfactant production if > 34w. Prevention: weekly IM injection of 17-OH progesterone caproate starting at 20w in women with history of previous idiopathic deliveries.

Premature Rupture of Membranes (PROM): Rupture of fetal membranes before onset of labor, whether at term or preterm.
Risk Factors: Ascending infection, local membrane defects and cigarette smoking. Presentation: history of sudden gush of copious vaginal fluid. On exam clear fluid is flowing out of vagina. Oligohydroamnios is seen on U/S. Diagnosis: sterile speculum exam meeting the following criteria: Pooling positive: clear watery amniotic fluid is seen in posterior vaginal fornix Nitrazine positive: fluid turns pH-sensitive paper blue Fern Positive: fluid displays fernning pattern on glass slide after air dry Chorioamnionitis is diagnosed clinically by maternall fever and uterine tenderness in presence of confirmed PROM and absence of URI or UTI. Hazards Associated with PROM: If Fetus Remains In Utero Neonatal Conditions: Infection and sepsis Deformation Umbilical cord compression Pulmonary hypoplasia Maternal conditions:
Chorioamnionitis, sepsis DVT

If Preterm Delivery Occurs Neonatal Conditions: ARDS (most common) PDA Intraventricular hemorrhage Necrotizing enterocolitis Retinopathy of prematurity Bronchopulmonary dysplasia Cerebral palsy

Management: If uterine contractions occur: tocolysis is contraindicated If Chorioamnionitis is present: obtain cervical cultures, start broad spectrum IV antibiotics and initiate prompt delivery If no infection: manage according to gestational age: o Before viability (<24w): outcome is dismal. Either induce labor or manage with bed rest at home.risk of pulmonary hypoplasia o Preterm viability (24-33w): conservative management. Hospitalize patient at bed rest, administer IM betamethasone if <32w, obtain cervical cultures and start 7d course of prophylactic ampicillin and erythromycin. o At term (34w): initiate prompt delivery. If vaginal delivery is expected, use oxytocin or prostaglandins as indicated. Otherwise, perform cesarean delivery.

Post-term Pregnancy: A pregnancy that continues for 40w/280d postconception OR 42w/ 294d after first day of LMP.
Etiology: mostly idiopathic, young primigravidas and rare with placental sulfatase deficiency. Pregnancy with anencephalic fetuses are the longest. Significance: Perinatal mortality increases due to changes in placental function over time. Macrosomia Syndrome: Mostly placental function continues resulting in healthy but large fetus. Cesarean rate is increased due to prolonged or arrested labor. Shoulder dystocia is more common with risks of fetal hypoxemia and brachial plexus injury. Dysmaturity syndrome: placental function declines as infarction and aging lead to placental scarring and loss of subcutaneous tissue. This reduction of metabolic and respiratory support to fetus can lead to asphyxia. Ceasarean rate is increased owing to nonreassuring fetal heart rate patterns. Oligohydramnios results in umbilical cord compression. Hypoxia results in acidosis & utero meconium passage. Management: Dates sure, favorable cervix: Management is aggressive. Induce labor with IV oxytocin and artificial rupture of membrane. Dates sure, unfavorable cervix: Management is controversial. Either aggressive with cervical ripening initiated with vaginal/cervical prostaglandin E2 followed by IV oxytocin OR conservative with twice weekly NSTs and AFIs awaiting spontaneous labor. Dates unsure: Management is conservative. Perform twice weekly NSTs and AFIs awaiting spontaneous labor. If fetal jeopardy is identified, delivery should be expedited. Management of Meconium: Previous recommendations to prevent meconium aspiration syndrome (MAS) included: In labor, amnioinfusion (with saline infused through an intrauterine catheter) to dilute meconium and provide fluid cushion to prevent umbilical cord compression. After head is delivered, suction fetal nose and pharynx to remove any upper airway meconium. After body is delivered, visualize vocal cords with a laryngoscope to remove meconium below vocal cords. AHA/AAP recommendations based on newer studies are: Amniofusion may be helpful to prevent MAS, okay to perform it. Suctioning of fetal nose and pharynx makes no difference in preventing MAS, do not perform routinely. Laryngoscopic visualization of vocal cords is only indicated if neonate is depressed; perform selectively.

Hypertensive Complications
HTN in Pregnancy
Systolic & diastolic BP both decline in T1, reaching a nadir by 24-28w, then gradually rise toward term but never return to pre-pregnancy baseline. Diastolic falls more than systolic, as much as 15mmHg. Arterial blood pressure is never normally elevated in pregnancy.

Gestational HTN
Sustained elevation of BP 140/90 after 20w pregnancy without proteinuria. BP returns to normal baseline postpartum. Presentation: no symptoms and unremarkable physical findings. Lab tests are remarkable. Proteinuria is absent. Management: Conservative outpatient management and close observation.

Mild Preeclampsia
Sustained elevation of BP >140/90 after 20w pregnancy with proteinuria 300mg/24h (1-2+), in absence of preexisting HTN. Risk factors: primiparas, multiple gestations, hydatidiform mole, diabetes mellitus, age extreme, chronic HTN & chronic renal disease. Presentation: excess weight gain and fluid retention. Hb, Hct, BUN, serum creatinine, serum uric acid and proteinuria. Managenment: The only definitive cure is delivery. Management depends gestational age: Before 36w: conservative inpatient management as long as mother & fetus are stable. No antihypertensive agents or MgSO4 are used. 36w: delivery with dilute IV oxytocin induction and continuous infusion of IV MgSO4 to prevent eclamptic seizures.

Severe Preeclampsia
Sustained elevation of BP 160/110 after 20w pregnancy with proteinuria 5g/24h (3-4+), in absence of preexisting HTN. OR presence of mild preeclampsia with evidence of maternal jeopardy: symptoms (headache, epigastric pain, visual changes), thrombocytopenia (<100000/ml), liver enzymes, DIC, pulmonary edema, oliguria (<750ml/24h) or cyanosis. Edema may or may not be present. Management: Aggressive prompt delivery is indicated at any gestational age with evidence of maternal or fetal jeopardy. Give IV MgSO4 5g, then 2g/h. Lower BP to diastolic values between 90-100 with IV hydralazine and/or labetalol. Attempt vaginal delivery with IV oxytocin if both stable. Conservative inpatient management may rarely be attempted in absence of maternal or fetal jeopardy at 26-34w if BP can be brought below 160/110 at ICU. Give continuous IV MgSO4 and maternal betamethasone.

Eclampsia
Unexplained grand mal seizures in a hypertensive, proteinuric pregnant woman in last half of pregnancy. Risk Factors: same as mild preeclampsia. A primary seizure disorder does not predispose to eclampsia. Etiology: Severe diffuse cerebral vasospasm resulting in cerebral perfusion deficits and cerebral edema. Presentation: same as mild and severe preeclampsia with unexplained tonic-clonic seizures. Management: Protect airway-tongue. Aggressive prompt delivery indicated at any gestational age after maternal/fetal stabilization. Give IV MgSO4 5g, then 2g/h. Lower BP to diastolic values of 90-100 with IV hydralazine and/or labetalol. Attempt vaginal delivery with IV oxytocin if both stable. Complications: intracerebral hemorrhage and even death.

Chronic HTN With/Without Superimposed Preeclampsia

Sustained HTN >140/90 with onset before pregnancy or 20w, +/- proteinuria. Pregnancy Prognosis with Chronic HTN: Good: If BP between 140/90 and 179/109, and no evidence of end organ damage. Poor: if renal disease(pregnancy loss if serum creatinine >1.4mg/dl), retinopathy & left ventricular hypertrophy (prolong BP >180/110) Worst: if uncontrolled HTN or chronic HTN with superimposed preeclampsia. Chronic HTN with Superimposed Preeclampsia: Chronic HTN along with documented rising BP values, worsening proteinuria or maternal jeopardy. Risk Factors: renal insufficiency, HTN for previous 4+ years and HTN in previous pregnancy Antihypertensive Drug Therapy Issues: Discontinue medications: if mild-moderate HTN because normal decrease in BP occur in pregnancy Maintain Medications: if severe HTN. Drug of choice is methyl-dopa. Labetalol & atenolol are alternatives (B are associated with IUGR) Never use medications: ACE inhibitors (fetal hypocalvaria, renal failure, oligohydramnios & death), diuretics BP target range: reduction of BP to normal levels may jeopardize uteroplacental blood flow. Maintain diastolic values between 90-100. Management: Conservative outpatient management: in uncomplicated mild-moderate chronic HTN. Stop drug therapy. Serial U/S and antenatal testing after 30w, serial BP and urine protein assessment. Induce labor at term if cervix is favorable. Aggressive prompt delivery at any gestational age: in chronic HTN with superimposed preeclampsia.

HELLP Syndrome
Hemolysis elevated liver enzymes and low platelets in preeclampsic patients. Risk Factors: multigravidas DDx: thrombotic thrombocytopenic purpura and hemolytic uremic syndrome Management: Prompt delivery at any gestational age and maternal corticosteroids. Complications: DIC, abruptio placenta, fetal demise, ascites and hepatic rupture.

Medical Complications in Pregnancy

Cardiac Diseases
Signs of heart disease include any diastolic or continuous heart murmur, any systolic murmur with a thrill, any severe arrhythmias and unequivocal cardiac enlargement. Maternal mortality risks are as follows: Low (<1%): ASD, VSD, PDA, minimal MS, porcine heart valve and corrected tetralogy of Fallot. Intermediate (5-15%): MS with AF, artificial heart valve, uncorrected tetralogy of Fallot, Marfan Syndrome with normal aortic diameter High (25-50%): pulmonary HTN, Eisenmengers syndrome, Marfan Syndrome with >40mm aortic diameter, peripartum cardiomyopathy Coronary Heart Disease: rare in childbearing age. Results in miscarriage, fetal death, preterm delivery and perinatal morbidity & mortality Rheumatic Heart Disease: Common acquired lesion in pregnancy is RHD, especially MS. Minimize tachycardia & excessive plasma volume. Congenital Heart Disease: ASD and VSD are tolerated well with pregnancy, as are any regurgitation lesions. Eisenmenger Syndrome: management is by avoiding hypotension. Peripartum Cardiomyopathy: Patient has no underlying heart disease, but develops idiopathic biventricular cardiac decompensation between last few weeks of pregnancy and first few months postpartum. Risks are advanced maternal age, multiparity, HTN & multiple pregnancy. Mortality rate is 75% if reversal does not occur within 6 months. Management is supportive in ICU. Specific Management of Cardiac Diseases: Antepartum: left lateral rest, 2g Na diet, digitalis & diuretics as indicated, avoid strenuous activity, avoid anemia, fetal ECHO Intrapartum: Aim for vaginal delivery, left lateral rest, monitor intravascular volume, O2, reassurance, sedation, SBE prophylaxis, epidural, no pushing, elective forceps to shorten second stage of labor, possible arterial line and pulmonary artery catheter (if marked limitations with activity) Postpartum: Watch for postpartum intravascular overload caused by sudden emptying of uterine venous sinuses after placental delivery.

Thyroid Disease
Normal thyroid physiology in Pregnancy: estrogen causes in TBG, thus total T3 & T4. Free T3 & T4 remain unchanged. Hyperthyroidism: etiology may be Graves disease, toxic nodular goiter (Plummer disease), hydatidiform mole or toxic diffuse goiter. If uncontrolled, it is associated with spontaneous abortions, prematurity, IUGR and perinatal morbidity and mortality. If controlled, pregnancy outcome is not altered. Clinic includes resting pulse, thyromegaly, exopthalmus, weight, total & free T4. Thyroid Storm presents with pyrexia, tachycardia & severe dehydration. Management is PTU, -Blockers, steroids and iodine. Graves Disease: its a common kind of hyperthyroidism in pregnancy with free T4, TSH and TSHR-Ab. Management: Antithyroid drugs are first line of therapy in pregnancy, but cross placenta and cause fetal hypothyroidism. PTU & methimazole are used. Subtotal thyroidectomy: performed in T2 if drugs fail Thyroid ablation with radioactive iodine (I 131) is contraindicated as it crosses placenta and destroys fetal thyroid. Hypothyroidism (TSH, free T4): Causes anovulation and infertility. If uncontrolled, it is associated with spontaneous abortion. If controlled with thyroid replacement, normal fertility and pregnancy outcomes are noted. Management: supplementary thyroid hormone

Seizure Disorders
Effect of pregnancy on seizure disorders: seizures worsen and anticonvulsant metabolism increases. Seizures cause maternal & fetal hypoxia. Effect of seizure disorders on pregnancy: pregnancy complications are minimal with prenatal care and compliance with anticonvulsants. Effect of anticonvulsans on fetus: congenital malformation rate, Risk of cerebral palsy, seizure disorders and mental retardation increase in offspring of epileptic women. Maternal phenytoin use is associated with neonatal deficiency of Vit-K dependent clotting factors: II, VII, IX & X. Management: Extra Folate supplementation before conception and during embryogenesis, Anomaly screening (offer triple-marker screen and T2 U/S), drug monotherapy (use single drug at lowest possible dose) and monitor anticonvulsant levels each trimester to prevent seizures

Liver Diseases
Intrahepatic Cholestasis of Pregnancy Intrahepatic cholestasis is stimulated by estrogen in genetically predisposed women in second half of pregnancy. Bile acids are incompletely cleared by liver and accumulate in plasma. Risk increases with multiple pregnancy. Preterm births & still births increase. Presentation: intractable pruritus on palms and soles of feet, worse at night, without specific skin finding. mildbillirubin & serum bile acids Management: Oral histamines (helpful in mild cases), Cholestyramine, Ursodeoxycholic acid (treatment of choice), antenatal fetal testing at 34w. Symptoms disappear after delivery. Acute Fatty Liver Life-threatening complication of pregnancy that occur in T3. Caused by deficiency in LCHAD enzyme. Presentation: Gradual onset of nonspecific flulike symptoms include nausea, vomiting, anorexia & epigastric pain. Jaundice, fever, HTN, proteinuria and edema. This progresses to acute renal failure, pancreatitis, hepatic encephalopathy and coma. liver enzymes, hyperbilirubinemia , DIC. Management: ICU stabilization with acute IV hydration and monitoring. Prompt delivery is indicated. Resolution follows delivery if mother survives.

Urinary Tract Infections

Most common organism is E.coli. Pregnancy itself is a risk factor. Asymptomatic Bacteriuria: most common UTI in pregnancy. If not treated, 30% develops acute pyelonephritis. No symptoms or signs. Diagnosis is made with positive urine culture showing >100K CFU of a single organism. Treated with single agnet, outpatient oral antibiotics. Acute cystitis: present with urgency, frequency and burning. No fever. Positive urine culture. Rest same as above. Acute Pyelonephritis: present with urgency, frequency, burning, fever, chills, costovertebral angle pain & tenderness, anorexia, nausea, vomiting and tachycardia. Preterm labor & delivery can occur. Severe cases are complicated by sepsis, anemia & pulmonary dysfunction, sometimes requiring ICU care, including intubation. Diagnosed with positive urine culture. Treated in hospital with IV hydration, parenteral antibiotics and tocolysis as needed.

Diabetes
A pregnant woman is unable to maintain fasting (FBS) or postchallenge glucose value in normal pregnant range before or after 100g glucose intake. Risk Factors: obesity, age>30y, family history, macrosomia, unexplained stillbirth or neonatal death, polyhydramnios, previous traumatic delivery. Classification: Gestational DM: onset during pregnancy, diagnosed in last half. Caused by diabetogenic effect of human placenta lactogen, placenta insulinase, cortisol & progesterone. 35% women with GDM will develop overt diabetes within 5-10y after delivery. Type 1 DM: is juvenile onset, ketosis prone, insulin-dependent diabetes caused by pancreatic islet cell deficiency. Type 2 DM: is adult onset, ketosis resistant, non-insulin-dependent diabetes caused by insulin resistance. Classification of Diabetes in Pregnancy: Class A1: GDM with normal FBS not requiring insulin Class A2: GDM with FBS requiring insulin Class B: Overt DM onset after age 20y and duration <10y. Class C: Overt DM onset age 10-19y or duration 10-19y Class D: Overt DM onset before age 10y or duration >20y Class E: Overt DM with calcified pelvic vessels Class F: Overt DM with nephropathy Class R: Overt DM with proliferative retinopathy. Screening: Who is screened? All pregnant women at 24-28w. In patients with risk factors, on first prenatal visit then repeated at 24-28w if initially negative. What is the test? 1h 50g oral glucose challenge test (OGTT) with normal values <140mg/dl. It does not need to be in fasting state. How to interpret? If 140, proceed to 3h 100g OGTT. If 200 and FBS 95, GDM is diagnosed and no further OGTT testing is needed. Diagnosis: 3h 100g OGTT is performed after overnight fast on all with abnormal screening test. 4 glucose values are obtained. Normal pregnant values are FBS<95, 1h <180, 2h <155, 3h <140. Impaired glucose tolerance is diagnosed if only one value is abnormal. GDM is diagnosed if atleast 2 values are abnormal. If FBS 125, overt diabetes is diagnosed and 100g glucose load should not be given. Antepartum General Management American Diabetic Association diet: educate patient to spread calories evenly throughout day, encouraging complex carboyhdrates. Home blood glucose monitoring: 4times/d with target values of FBS <90 and 1h after meal of < 140 Insulin Therapy: start subcutaneous insulin in all 3 forms of DM if values are above target range. Total daily insulin units = actual body weight x 0.8 (T1), 1 (T2), 1.2 (T3). Take 2/3 of total daily dose in morning and 1/3 in evening. Oral hypoglycemic agents: Glyburide in GDM not controlled with diet. Antepartum Overt Diabetes Management: Hemoglobin A 1C: obtain a level on first visit and repeat each trimester Renal Status: obtain an early pregnancy baseline 24h urine collection for total protein and creatinine clearance Retinal status: obtain an early pregnancy ophthalmologic funduscopic evaluation for proliferative retinopathy. Home Blood Glucose Monitoring: at least 4/d with target values of FBS 60-90 mg/dL & 1h after meal of <140 mg/dL. Preconception Anomaly Prevention: overt diabetes is associated with fetal anomalies. Maintaining normal glucose values, starting 3m prior to discontinuing contraception reduces the anomaly risk to that of non-diabetes. Folic Acid 4mg/d should be started 3m prior conception. Antepartum Fetal Assessment: Anomaly Screening: Anomalies are not increased in GDM because hyperglycemia is not present in first half of pregnancy. Most common fetal anomalies with overt DM are NTD and congenital heart disease. An uncommon anomaly, but one highly specific for overt DM, is caudal regression syndrome. Obtain a triple-marker screen at 16-18w to assess for NTD and targeted ultrasound at 18-20w to assess for structural anomalies. If glycosylated hemoglobin is elevated, order a fetal ECHO at 22-24w to assess for congenital heart disease. Fetal Growth: Monthly sonogram will assess fetal macrosomia (common) or IUGR (seen with longstanding DM & vascular disease). Fetal Surveillance: Start weekly NST & AFI at 25w if small vessel disease or poor glycemic control is present OR at 32w if taking insulin, macrosomia, previous still birth or HTN. Biophysical profiles can be performed during monthly U/S. Intrapartum Management: Delivery Timing: Fetal maturity is delayed in diabetic mothers, yet proloningin pregenancy increases risk of stillbirth. Target delivery age is 40w, but may be earlier in presence of fetal jeopardy and poor maternal glycemic control. An amniotic fluid lecithin to sphingomyelin ration (L/S) of 2.5 in presence of phosphatidyl glycerol assures fetal lung maturity. Mode of Delivery: C-section rate is 50% due to macrosomia, arrest of labour and concern regarding shoulder dystocia. Glycemic Control: Maintain blood glucose levels between 80 & 100 mg/dL using 5% dextrose in water and an insulin drip. Postpartum Management: Postpartum Hemorrhage: watch for uterine atony related to overdistended uterus. Hypoglycemia: turn off insulin infusion because insulin resistance decreases with rapidly falling levels of hPL after delivery of placenta. Neonatal Problems: Hypoglycemia: caused by persistant hyperinsulinemia from excessive prenatal transplacental glucose. Hypocalcemia: caused by failure to increase parathyroid hormone synthesis after birth. Polycythemia: caused by elevated erythropoietin from relative intrauterine hypoxia. Hyperbillirubinimia: caused by liver immaturity and breakdown of excessive neonatal RBC Respiratory Distress Syndome: caused by delayed pulmonary surfactant production.

Anemia (Hb <10g/dL during pregnancy or puerperium)

Iron deficiency Anemia: most common anemia in women due to menstruation and pregnancy
Diagnosis: Microcytic hypochromic RBC, Hb <10 gdL, MCV< 80, RDW>15% Pregnancy Requirements: 800mg of elemental iron, of which 500mg goes to expand RBC mass and 300mg to fetal-placental unit. Risk Factors: chronic bleeding, poor nutrition, frequent pregnancies Symptoms: none to general malaise, palpitations and ankle edema Fetal Effects: none Treatment: FeSO4 325mg pot id Prevention: elemental iron 30mg/d

Folate Deficiency Anemia

Diagnosis: macrocytic RBC, Hb g/dL, MCV >100, RDW >15, RBC folate levels are low. Peripheral smear may show hypersegmented neutrophils. Risk Factors: chronic hemolytic anemia (sickle cell disease), anticonvulsant use (phenytoin, phenobarbital) & frequent pregnancies. Symptoms: none to general malaise, palpitations and ankle edema Fetal Effects: LBW, increase NTD Treatment: Folate 1mg po daily Prevention: Folate 0.4 mg po daily for all women, 4mg po daily for those at high risk for NTD

Sickle Cell Anemia

Screening Test: peripheral blood test for presence of Hb S. Diagnostic Test: Hb electrophoresis will differentiate between SA trait or SS disease. Risk Factors: African and Mediterranean descent Effects on Pregnancy: increased UTI with SA trait and spontaneous abortion, IUGR, fetal deaths and preterm delivery with SS disease Treatment: Avoid hypoxia, take folate supplements and monitor fetal growth and well being

Thrombophilias
These are disorders that promote blood clotting. Pregnancy itself is a risk factor for thrombophilia. Most women with thrombophilia have healthy pregnancies; however it may contribute to T1 miscarriages, T2 T3 stillbirths, placental abruption and severe preeclampsia. They are also at high risk for VTE. Pulmonary embolism m is leading cause of maternal death in US. Factor V Leiden and prothrombin mutation are common inherited thrombophilia. Antiphospholipid syndrome (APS) is acquired thrombophilia causing 15% of repeated miscarriages. Diagnosis: Following tests recommended to pregnant women with blood clot, positive family history (thrombosis, PE or stroke prior to 60y) and history of complications (2 misscarriages, stillbirth, early or severe preeclampsia, placental abruption, poor fetal growth due to unknown cause): Factor V Leiden and prothrombin 20210 gene mutation Hyperhomocysteinemia Deficiency of antithrombin III, protein C and protein S Antiphospholipid syndrome Treatment: Subcutaneous low molecular weight heparin (some cases low dose aspirin is also given along heparin) and monitoring of anticoagulation. No anticoagulation is required in less severe type of thrombophilias & no history of blood clots or pregnancy complications. Postpartum Warfarin for 6-8w is recommended for all patients. It is safe during breastfeeding but contraindicated antepartum. Thromboembolism The mediating factor is frequently the endothelial injury from traumatic delivery or C-section. In postpartum period, risk increases 5 folds. Vascular stasis is strongest predisposing factor with decreased pelvic and lower extremity blood flow. Enhanced coagulability in pregnancy is due to increased factor II, VII, VIII, IX and X. Superficial Thrombophlebitis: does not predispose to thromboembolism. There is localized pain and sensitivity, tenderness, erythema and swelling. Diagnosis is made when DVT is ruled out. Management is conservative with bed rest, local heat and NSAIDs. DVT: predispose to thromboembolism and site of thrombosis is typically the lower half of body (50% in pelvic veins and 50% in lower extremity). There may be no complaints OR pain, increased skin sensitivity and calf pain on foot dorsiflexion (Homan Sign). Diagnosis is made by duplex Doppler (above knee) or venography (below knee). Treatment is IV heparin to increase PTT by 1.5-2.5 times the control value. Subcutaneous heparin is used once therapeutic levels are achieved. No warfarin antepartum. Thrombophilia workup is followed. Pulmonary embolism: fatal result of DVT. There is chest pain, dyspnea, tachypnea, often normal chest X ray, ABG with low pO2 (often normal), ECG may show tachycardia, right axis deviation (usually normal). Spiral CT of chest is best initial test of suspected PE. Pulmonary angiography is definitive diagnostic test (indication is negative spiral CT in a high risk & symptomatic patient). Treat as DVT.

Anatomy Of pelvis
4 Bones: ilium superior-laterally, ischieum inferior-laterally, pubis antirorly and sacrum & coccyx posteriorly st 4 Joints: bilateral sacroiliac joints, symphysis pubis & sacrococcygeal joint. (Sacral promonotory = ant sup edge of 1 sacral vertebra Landmarks: Pelvis is divided by linea terminalis into false pelvis above & true pelvis below. False pelvis is bordered by lumber vertebrae posteriorly, iliac fossa laterally & abdominal wall anteriorly. True pelvis is a bony canal formed by posterior sacrum & coccyx, lateral ischial and anterior pubis.

Types of Pelvic Shapes:

Gynecoid: classic female pelvis with round oval inlet found in 50% women. Pelvis is spacious for fetal head to pass Android: typical male pelvis with triangular inlet found in 30% women. Pelvis is restricted in all levels. Arrest of descent is common. Anthropoid: resembles pelvis of apes and inlet is larger anterior-posteriorly with side walls that converge. Fetal head engages anterior-posteriorly, often in occiput posterior position, making delivery difficult. Platypelloid: flattened gynecoid pelvis with elongated transverse oval inlet. Fetal head engages transverslly & delivers occiput transverse position.

Fetal Orientation in Utero

Lie: orientation of long axis of fetus to that of uterus Longitudinal: fetus and mother are in same vertical axis. Most common lie. Transverse: fetus at right angle to mother Oblique: fetus at 45 angle to mother. Presentation: portion of fetus overlying pelvic inlet. Common is cephalic Cephalic: head presents first Breech: feet or buttocks present first. Major risk of vaginal breech delivery is entrapment of after coming head. o Frank: thighs are flexed & legs extended. Potentially could be safely delivered vaginally o Complete: thighs & legs flexed o Footling: thighs & legs are extended Compound: more than one part presents Shoulder: presents first Position: relationship of a definite fetal part to maternal body pelvis. Common is occiput anterior. Occiput: with a flexed head (cephalic presentation) Sacrum: with a breech presentation Mentum (chin): with an extended head (face presentation) Attitude: degree of extension-flexion of fetal head. Vertex (head maximally flexed, common), military (head is partially flexed), brow (head is partially extended) and face (head is maximally extended). Station: degree of descent of presenting part through birth canal, expressed in cm above or below maternal ischial spine. Synclitism: condition of parallelism between the plane of pelvis and that of fetal head.

Overview of Labor
Cervical Effacement: uneffaced (0%) cervix is 2cm long and 2cm wide, fully effaced (100%) cervix has no length and is paper-thin Cervical Dilation: 1-10cm

Stages of Labor
Stage 1: Latent phase effacement Prepares cervix for dilation Stage 1: Active phase dilation Rapid cervical dilation Stage 2: Descent of fetus Stage 3: expulsion of placenta Begins: onset of regular uterine contraction Ends: acceleration of cervical dilation Begins: acceleration of cervical dilation Ends: 10cm Begins: 10cm Ends: delivery of baby Begins: delivery of baby <20h in primipara <14h in multipara 1.2 cm/h primipara 1.5 cm/h multipara <2h in primi, <1h in multi, add 1h if epidural <30min

Conduct of Normal Spontaneous Labor

Preadmission: NO admission to maternity unit until cervical dilation is at least 3cm, unless PRM occurred. Cephalic presentation. Admission: open IV, oral clear liquid may be ingested and lateral recumbent position encouraged. First Stage: assess fetal HR with continuous electronic monitoring. Appropriately spaced vaginal exam to check dilation and head descent. Amniotomy performed in active phase when fetal head is well applied to cervix. Analgesia administered at patient request. Second & Third Stage: episotomy is not routine but performed as indicated. After delivery, administer IV oxytocin and allow spontaneous separation of placenta. Recovery Period: observe closely for bleeding and development of preeclampsia for first 2h postpartum.

Abnormal Labor
Prolonged Latent Phase: mostly due to injudicious analgesia. Also due to hypotonic or hypertonic contractions. Diagnosis: cervix dilation 3cm, acceleration phase of dilation not reached. No cervical change in 14h. Management: therapeutic rest and sedation Prolonged or Arrested Active Phase: Causes: either abnormality of passenger (large fetal size, abnormal fetal orientation in uterus), pelvis (bony pelvic size) or power (dysfunctional or inadequate uterine contractions). Diagnosis: cervix dilation 3cm, acceleration phase of dilation reached. Prolonged (2cm change in 4h), arrest (no change in 3h). Management: Assess uterine contraction quality. Contractions should occur every 2-3min, last 45-60 sec with 50mmHg intensity. If contractions are hypotonic (inadequate frequency, duration or intensity): give IV oxytocin, if hypertonic (high intensity but inadequate duration or frequency): give morphine, if adequate contractions: emergency C-section. Prolonged Second Stage: causes as above Diagnosis: 10cm dilation at +1 station but no descent change in 3h Management: Assess contractions and maternal pushing efforts. Use IV oxytocin or enhanced coaching as needed. If both are adequate, assess fetal head, if not engaged: emeregency c-section, if engaged: try either obstetric forceps or vaccum extractor. Prolonged Third Stage Causes: inadequate contractions. If placenta did not separate inspite of IV oxytocin, think of abnormal placental implantation. Diagnosis: failure to deliver placenta within 30min Management: manual placental removal or rarely even hysterectomy

Prolapsed Umbilical Cord: obstetric emergency Occult: cord has not come through cervix but is compressed between feral head and uterine wall. Partial: cord is between head and dilated cervical os but not protruded into vagina Complete: cord has protruded into vagina Risk Factors: rupture of membrane with presenting part not applied firmly to cervix, malpresentation. Diagnosis: amniotomy at 2 station and severe variable decelerations Management: Do not hold the cord or try to push it back into uterus. Place patient in knee chest position, elevate presenting part, avoid palpating the cord and perform immediate C-section. Shoulder Dystocia: Delayed delivery of fetal shoulders after delivery of head. Usually associated with fetal shoulders in ant-post plane, with anterior shoulder impacted behind pubic symphysis. Results in permanent neonatal neurologic damage in 2% cases. Risk Factors: maternal diabetes, obesity and postdates pregnancy which are associated with fetal macrosomia. 50% occur in <4kg Management: suprapubic pressure, maternal thigh flexion (McRoberts maneuver), internal rotation of shoulders to oblique plane (Woods corkscrew maneuver), manual delivery of posterior arm and Zavanelli maneuver (cephalic replacement). Obstetric Lacerations First Degree: only vaginal mucosa. Suture reoair is often not needed. Second Degree: vagina and muscles of perineal body but not anal sphincter. Suturing is necessary. Third Degree: vagina, perineal body and anal sphincter but not rectal mucosa. Suturing is necessary to avoid anal incontinence Fourth Degree: vagina through rectal mucosa. Complications of faulty repair or healing include rectovaginal fistula. Episiotomy Possible Indications: shoulder dystocia, non-reassuring fetal monitor tracing, forceps or vacuum extractor vaginal delivery, vaginal breech delivery and narrow birth canal. Not routinely practiced. Midline or mediolateral surgical incision is done.

Obestetric Analgesia
IV Agents: these are narcotics and sedatives given in active phase. Disadvantage: neonatal depression if given close to delivery and neonate may need Naloxane to reverse the effects. Paracervical Block: bilateral transvaginal local anesthetic injection to block Frankenhausers ganglion lateral to cervix in active phase. Disadvantage: transitory fetal bradycardy which is managed conservatively. Pudendal Block: bilateral transvaginal local anesthetic injection to block pudendal nerve in stage 2 Epidural Block: injection of anesthetic in epidural space to block lumbosacral nerve roots during stages 1& 2. Disadvantage: patchy block from nonuniform spread. Complications: hypotension, spinal headache, CNS bleeding/infection. Hypotension is treated with IV fluids & IV ephedrine. Spinal headache treated with IV hydration, caffeine or blood patch. Spinal Block: injection in subarachnoid space to block lumbosacral nerve roots during stage 2 & C-section. Complication as above. GA: seldom used in vaginal delivery and rarely for C-section. Indications are need for rapid emergency delivery, maternal medical conditions where conduction anesthesia is unsafe (blood dyscrasia, thrombocytopenia). Complications: aspiration pneumonia, atelectasis and uterine atony (associated with halothane, enflurane)

Antepartum Fetal Testing

Common reasons are decreased fetal movements, diabetes, post-dates, chronic HTN and IUGR.

Nonstress Test (NST): assesses frequency of fetal movements and uses external FHR monitor to detect presence or absence of accelerations.
Reactive NST: 2 accelerations in 20 min. this is reassuring and highly predictive of fetal well being. Repeat NST weekly. Nonreactive NST: when above criteria is not met. 80% are false positive due to fetal sleep, prematurity, drug effects & CNS anomalies. Perform fetal vibroacoustic stimulation. If NST is persistently nonreactive, perform biophysical profile or contraction stress test.

Amniotic Fluid Index: <5cm = oligohydramnios, 5-8cm = borderline, 9-25cm = normal, >25cm = polyhydramnios Biophysical Profile (BPP): It measures 5 components of fetal wellbeing: NST, amniotic fluid volume, fetal gross body movement, fetal extremity tone, and fetal breathing movements. Last 4 components are assessed using obstetric ultrasound. Score of 0-2 is given for each component.

8-10: highly reassuring of fetal well being. Repeat test weekly. 4-6: worrisome. Deliver if 36w. Repeat BPP in 12-24h if <36w or perform CST. 0-2: fetal hypoxia. Prompt delivery regardless of gestational age. A modified BPP includes only NST and amniotic fluid volume. Its predictive value is almost as high as a complete BPP. Contraction Stress Test (CST): assesses the ability of fetus to tolerate transitory decreases in intervillous blood flow that occur with uterine contraction. It uses both external FHR & contraction monitoring devices and is based on presence or absence of late deceleration. If 3 contractions in 10min are not spontaneously present, induce it with either IV oxytocin or nipple stimulation. This test is rarely performed because of cost and time required. Most common indication is a BPP of 4 or 6. Negative CST: absence of late deceleration with contractions. This is highly reassuring. Repeat CST weekly. Positive CST: presence of late deceleration with at least 50% contractions. 50% false positive. Perform prompt delivery. Contraindication: when contractions are hazardous to mother or fetus (previous classical uterine incision, previous myomectomy, placenta previa, incompetent cervix, PMR and preterm labor. Umbilical Artery Doppler: measures ratio of systolic & diastolic blood flow in umbilical artery. Umbilical circulation has low resistance, so diastolic blood flow is expected. S/D ratio normally decreases throughout pregnancy. It is predictive of poor perinatal outcome only in IUGR fetuses. Absence of diastolic flow and reversed diastolic flow is non-reassuring and need delivery.

Intrapartum Fetal Monitoring

Fetal Heart Rate Monitoring
Done with fetoscope or electronic monitoring with similar outcome. External Devices: placed on fundus. Advantage: utilization before significant cervical dilation and membrane rapture. Disadvantage: poor quality with maternal obesity and maternal discomfort from device belts. Fetal: continuous U/S transducer picks up fetal cardiac motion and maternal great vessel pulsation Contractions: tocographic transducer senses change in uterine wall muscle tone. It measures beginning & end of contractions but cannot assess contraction intensity. Internal Devices: placed through dilated cervix. Advantage is optimum quality. Disadvantage is limitation to labor. Fetal: direct scalp electrode senses each QRS complex of fetal cardiac cycle. Complication include fetal scalp trauma & infection. Contractions: IUPC placed on uterine cavity registers intrauterine hydrostatic changes with each contraction. Evaluation Baseline HR: this is mean FHR during 10min. normal values are between 110-160 beat/min. Bradycardia: <110 beat/min. non-reassuring. Nonhypoxic explanations are maternal -blocker or local anesthetic, or congenital heart block. Tachycardia: >160 beat/min. non-reassuring. Nonhypoxic explanations are maternal (-agonists like terbutaline, ritodrine, fever, thyrotoxicosis) and fetal (repetitive acceleration from movement, fetal arrhythmia and prematurity.) Periodic Changes Acceleration: abrupt increase in FHR above baseline lasting <2min and are unrelated to contractions. The criteria vary by gestational age: Before 30w: 10 beats/min lasting 10s. After 30w: 15 beats/min lasting 15s. Acceleration occurs in response to fetal movement and are reassuring. Early Deceleration: gradual decrease in FHR below baseline beginning and ending simultaneously with contractions. They are mediated by vagal stimulation and occur in response to fetal head compression. Early decelerations have no impact on clinical outcome. Variable Deceleration: abrupt decrease in FHR below baseline of at least 15 beats/min with onset to nadir of <30s. They are variable in relation to contractions. They are mediated by vagal stimulation and occur in response to umbilical cord compression. Mild variables drop 15-40 beats/min. Moderate variables drop 40-60 beats/min. Severe variable drop >60 beats/min or last 60s. Mild to moderate variables have no impact on clinical outcome. Severe variables are non-reassuring and may be associated with fetal acidosis. Late Deceleration: gradual decrease in FHR below baseline with onset to nadir of 30s. Deceleration onset and end is delayed in

relation to contractions. Mediated by either vagal stimulation or myocardial depression and in response to uteroplacental insufficiency. All late decelerations are non-reassuring and may be associated with fetal acidosis.
Variability These are baseline FHR fluctuations in amplitude and frequency of 2 cycles/min. Variability is a reflection of normal healthy autonomic interplay between sympathetic and parasympathetic nervous system. Absent: no variability. This is nonreassuring Minimal: 5 beats/min Moderate: 6-25 beats/min. this is considered normal variability. Marked: >25 beats/min Criteria for Reassuring FHR Tracing: Baseline rate is between 110-160 beats/min. Acceleration and variability are present. Deceleration is absent. Criteria for Nonreassuring FHR Tracing/fetal distress: Baseline rate show tachycardia or bradycardia without explanation. Accelerations are absent. Repetitive variable decelerations, if severe, are seen. There are repetitive late decelerations of any magnitude. Variability is absent. Intrauterine Resuscitation Decrease uterine contraction: turn off IV oxytocin infusion or give subcutaneous 0.25mg Terbutaline to enhance placental blood flow. Augment IV fluid volume: infuse 500ml bolus IV normal saline rapidly to enhance uteroplacental infusion Give high-flow 8-10L Oxygen by facemask. Amniofusion: to eliminate severity of variable deceleration. Change position from supine to lateral or from one lateral position to other later side. Perform digital vaginal exam to rule out possible prolapsed umbilical cord. Perform digital scalp stimulation observing for acceleration, which would be reassuring of fetal condition.

Fetal pH Assessment
Intrapartum fetal scalp blood pH: may be used if EFM strip is equivocal. Prerequisites include cervical dilation, ruptured membranes, and adequate descent of fetal head. Contraindications are suspected fetal blood dyscrasia. Blood is obtained from fetal scalp incision. Normal pH 7.2 Postpartum umbilical artery blood pH: used to confirm fetal status at delivery. Umbilical cord venous and arterial blood is sampled. Approach to Nonreassuring Fetal Monitoring Tracing Examine EFM strip looking for baseline FHR, degree of variability and presence of periodic changes. Confirm abnormal findings (reassuring criteria) Identify nonhypoxic causes present that could explain the abnormal findings. Initiate intrauterine resusciatation measures and observe for normalization of EFM tracing Prepare for delivery promptly if resuscitation measures do not normalize EFM tracing. Specific interventions if immediate delivery is indicated: in stage one of labor, only option is emergency C-section. In stage two, operative vaginal delivery (vacuum or forceps) may be appropriate, or an emergency C-section must be performed.

Operative Obstetrics
Any method used to deliver fetus other than uterine contractions and maternal pushing efforts. It includes vaginal or cesarean.

Obstetric Forceps
Simpson (for traction only), Kjelland (for head rotation and traction), Piper (for after-coming head of a vaginal breech baby) and Barton (for delivery of head in occiput transverse position with a platypelloid pelvis). Classification Outlet: fetal head is on pelvic floor. Most forceps use in this category Low: Fetal head is below +2 station, but has not reached pelvic floor. Mid: fetal head is below 0 station. This is seldom used today. High: fetal head is not engaged. Never appropriate Indications: prolonged second stage (most common), nonreassuring EFM strip, avoid maternal pushing and breech presentation. Prerequisites: adequate pelvic dimensions, experienced operator, full cervical dilation, engaged fetal head, certainty of fetal head orientation. Complications: laceration of vagina/cervix/perineum/uterus, soft tissue compression or cranial injury.

Vacuum Extractor
Advantages over Forceps: Precise knowledge of fetal head position and attitude is not essential. Vacuum does not occupy space adjacent to fetal head rd th 3 & 4 degree lacerations are fewer. Fetal head rotation occurs spontaneously at station best suited to fetal head configuration and maternal pelvis. Disadvantage: cup pop-offs, scalp trauma, subgaleal hemorrhage & intracranial bleeding (rare), neonatal jaundice from bleeding. Indications: similar to forceps Prerequisites: similar to forceps except certainty of fetal head orientation, also gestational age should be 34w. Complications: vaginal laceration, neonatal cephalohematoma & scalp lacerations (common), subgaleal hematoma or intracranial hemorrhage although uncommon, are associated with vacuum duration >10min.

Cesarean Section
Risks: hemorrhage (1000ml) twice vaginal delivery, infection, visceral injury and DVT. Maternal mortality & morbidity is higher than vaginal delivery, especially if performed in labor. Maternal mortality is mostly anesthetic related. Uterine Incisions: Low Segment Transverse: common, bladder must be dissected off, low chance of uterine rapture in next labor. Advantge: trial of labor in next pregnancy is safe, risk of bleeding & adhesion is low. Disadvantage: fetus must be longitudinal lie, lower segment must be developed. Classis: less common, easy to perform, no bladder dissection needed. Significant risk of uterine rapture before labor and in next labor. Repeat C-section should be scheduled before labor onset. Advantage: orientation not important, lower segment varicosities or myomas can be bypassed Disadvantage: trial of labor in next pregnancy is unsafe, risk of bleeding and adhesions are higher.

Postpartum Issues
Lochia: layers of endometrial decidua shred during first 3w postpartum. Initially red (lochia rubra) first few days, then pink(lochia serosa) and ending with white (lochia alba) by the end of second week. Cramping: myometrial contractions, managed by mild analgesics. Perineal Pain: minimize discomfort from episiotomy/lacerations in first 24h with ice packs and after d1 with heat lamp or sitz bath. Hypotonic Bladder: if postvoid residual volume>250ml, give bethanechol (Urecholine). Foley may also be needed for few days. Dysuria: due to Intrapartum catheterization. urinary analgesic may be needed. Constipation: oral hydration and stool softeners Hemorrhoids: prolong second stage pushing efforts exaggerate it. oral hydration and stool softeners Impaired Maternal-infant Bonding: mother shows no interest for baby, seen in first few days especially if baby is in NICU or poor social support. Manage by psychosocial evaluation and support. Postpartum Blues: mood swings and terafulness first few days. Normal physical activity and care for self and baby continues. Conservative management with social support. Postpartum Depression: feeling of despair and hopelessness frequently delayed upto a month (21d). Patient does not get out of bed with care for self and baby neglected. Managed by psychotherapy and antidepressants. Postpartum Psychosis: loss of reality & hallucinations within first few weeks (21d). Hospitalize, psychotherapy and antipsychotics.

Postpartum Contraception & Immunization

Breast Feeding: lactation is associated with temporary anovulation, so may deffere contraceptive use for 3m. Diaphragm: fitting should be performed at 6w postpartum visit. IUD: at 6w postpartum visit Combination Pill: should not be used in breast feeding women as estrogen diminishes milk production, nonlactating, start after 3w. Progestin Contraception: can be started immediately after delivery. RhoGAM: if mother is Rh (D) negative & baby positive, give 300g IM within 72h of delivery. Rubella: if mother is rubella IgG Ab negative, give active rubella immunization and avoid pregnancy for 1m to avoid fetal infection.

Postpartum Hemorrhage
Uterine Atony: common cause of postpartum bleeding (50%) Risks: rapid or protracted labor (most common), Chorioamnionitis, medications (MgSO4, -adrenergic agonists, halothane), over distended uterus Clinic: soft dough like uterus palpable above umbilicus Management: uterine massage and uterotonic agents (oxytocin, methylergonovine, or carboprost. ) Lacerations: (20%) Risks: uncontrolled vaginal delivery (common), difficult delivery and operative vaginal delivery. Clinic: identifiable cervical/vaginal/perineal laceration in presence of contracted uterus Management: surgical repair First degree: perineal mucosa: manage conservatively if not bleeding Second degree: perineal muscles only: Third degree: rectal sphincter also Fourth degree: rectal mucosa (careful suturing to avoid rectovaginal fistula formation) Retained Placenta (10%) Risks: Accessory Placenta Lobe (common), abnormal trophoblastic uterine invasion Clinic: missing placental cotyledons in presence of contracted uterus Management: Manual removal or uterine curettage under ultrasound guidance. DIC (Rare) Risks: Abruptio placenta, severe preeclampsia, amniotic fluid embolism and prolonged retention of a dead fetus. Clinic: generalized oozing or bleeding from IV sites or lacerations in presence of contracted uterus Management: Removal of pregnancy tissues form uterus, ICU support and selective blood product replacement. : Uterine Inversion (rare) Risk: myometrial weakness (common) and previous uterine inversion. Clinic: beefy appearing bleeding mass in vagina and failure to palpate uterus vaginally. Management: uterine replacement by elevating vaginal fornices and lifting uterus back into its normal position, followed by IV oxytocin. Unexplained: Laparatomy and bilateral ligation of uterine or internal iliac arteries. Hysterectomy would be a last resort.

Postpartum Fever
PP Day 0: Atelectasis Risk: general anesthesia with incisional pain (common) and cigarette smoking Clinic: Mild fever with mild rales on auscultation. Unable to take deep breaths Management: Pulmonary exercises and ambulation. CXR are unnecessary. PP Day 1-2: UTI Risks: multiple Intrapartum catheterizations and vaginal exam due to prolong labor Clinic: High fever, costovertebral flank tenderness, positive urinalysis and urine culture Management: single agent IV antibiotics PP Day 2-3: endometritis (common cause) Risks: emergency C-section after prolonged membrane rapture and prolonged labor Clinic: moderate to high fever with uterine tenderness. Absent peritoneal signs and decrease peristalsis Management: multiple agent IV antibiotics (gentamycin+clindamycin) PP Day 4-5: wound Infection Risk: Emergency C-section after prolonged membrane rupture and prolonged labor Clinic: Persistent spiking fever despite antibiotics, along with wound erythema, fluctuance or drainage Management: IV antibiotics for cellulitis. Wound drainage with twice-daily wet to dry wound packing used for an abscess, secondary closure PP Day 5-6: septic Thrombophlebitis Risks: Emergency C-section after prolonged membrane rupture and prolonged labor Clinic: persistent wide fever swings despite broad spectrum antibiotic with normal pelvic and physical exam Management: IV heparin for 7-10d, keeping PPT values at 1.5 to 2 times baseline PP Day7-21: Infectious Mastitis Risk: lactational nipple trauma and cracking allowing entry of staphylococcus into breast ducts and lobes Clinic: fever of variable degree with localized, unilateral breast tenderness, erythema and edema Management: Oral Cloxacillin. Breast feeding can be continued.

Benign Breast Disorders

Cystic Breast Mass: Diagnosis: Cyst aspiration and fine needle aspiration are important in diagnosis of breast disorders. Management: Preaspiration mammography should be obtained. If cyst disappears and cytology is benign, no further workup is required. Fibrocystic Breast Changes Diagnosis: fibroadenomas are common in young women and as multiple lesions. Common in upper outer quadrant.No association with cancer. Cysts and fibroadenomas may be indistinguishable on palpation, but U/S easily distinguishes solid from cyst. On fine needle aspiration, cyst collapse while samples from fibroadenoma present as combination of epithelial and stromal elements. Management: conservative if sure of diagnosis by U/S and core-needle/fine needle aspiration. May resolve. But mostly patients prefer excisional biopsy. Lesion is shelled out with surrounding thin rim of breast tissue (safe side if it turn out to be phyllodes tumor) Mammography Micro-calcifications: Diagnosis: mostly benign lesions and nonpalpable but 20% represent early cancer. Requires stereotactic needle localization and core biopsy under mammographic guidance. Treat based on histologic diagnosis. Persistent Breast Mass: even after fine needle biopsy. Excisional biopsy is recommended: Cellular bloody cyst fluid on aspiration Failure of suspicious mass to disappear completely upon fluid aspiration Bloody nipple discharge, with or without a palpable mass Skin erythema & edema suggesting inflammatory breast carcinoma and needle core biopsy could not be performed. In past, recurrent or persistent simple breast cysts were routinely excised. Because of improvements in U/S, these are followed conservatively. Bloody Nipple Discharge Usually due to intraductal papilloma and treatment is total excision of duct and papilloma through circumareolar incision. Modern ductography is used only in identifying multiple lesions or lesions in periphery of breast.

Breast Cancer

Gynecologic Procedures
Cervical Pap Smear: OPD procedure, a screening test, NOT diagnostic test for premalignant changes. (Diagnosis require tissue specimen)
It includes cytologic specimens of transformation zone and endocervical canal. A plastic spatula is rotated against T-zone and a brush (cotton tipped applicator in pregnancy) is used to obtain ECC cells. Colposcopy: OPD procedure, where a binocular is used to examine exocervix through a speculum, to localize areas of abnormal epithemium. Cold Knife Cone Biopsy: minor outpatient surgical procedure performed in operating room under LA or GA. It is a diagnostic test to examine histology of cervical lesions. A cone shaped tissue from cervix is obtained with scalpel. Risks are cervical stenosis and cervical insufficiency. Loop Electrosurgical Excision procedure (LEEP): minor outpatient surgical procedure performed under LA. A diagnostic test to examine histology of cervical lesions, used for diagnosis & treatment of cervical dysplasia. Follow up Pap smears are done every 6m for 2y. Risks like above. Cryotherapy: OPD procedure without anesthesia. It destroys dysplastic cervical tissue identified by colposcopy and cervical biopsy. A watery discharge will occur over next few weeks. Follow up Pap smears are done every 6m for 2y. Risks include cervical stenosis. Hysterectomy: Performed in OR under RA/GA for diagnosis and therapy. Performed vaginally or abdominally. Subtotal (only corpus of uterus), total (corpus & cervix) and radical (performed for early stage cervical carcinoma, removes corpus, cervix, proximal vagina and broad ligaments). Hysteroscopy: minor outpatient surgical procedure done in OR under LA/GA for diagnosis and possibly for therapeutic purpose. Laparscopy: minor outpatient surgical procedure done in OR under GA for diagnosis and possibly for therapeutic purpose. Gynecologic indications include diagnosis and treatment of chronic PID, resecting advance ectopic pregnancies and diagnosing and lysing tubal adhesions in infertility. Hysterosalpingogram (HSG): Diagnostic outpatient radiologic imaging done without anesthesia for uterine malformations and tubal pathology. D&C: minor outpatient surgical procedure done in OR under LA/GA. Its adiagnostic test that examines histology of endometrial lesions. D&E: minor outpatient surgical procedure done in OR under LA/GA for removal of fetus (in parts) and placental tissue in advanced pregnancy. Endometrial/Vulvar Biopsy: OPD procedure with topical anesthesia. It is a diagnostic test to examine histology of endometrial/vulvar lesions.

Pelvic Relaxation
Commonly due to child birth. Diagnosis is made by pelvic examination and observation of prolapsed vagina, rectum and uterus. Uterine Prolapse: Grade I (cervix descends halfway), II (cervix descends to introitus), III (cervix extends outside introitus), IV/procidentia (entire uterus and anterior & posterior vaginal walls extends outside introitus. Cystocele: herniation of anterior vaginal wall and underlying bladder base into vaginal lumen. Mostly postmenopausal with urinary incontinence. Rectocele: herniation of posterior vaginal wall and underlying rectum into vaginal lumen. postmenopausal with digitally assisted removal of stool. Enterocele: herniation of pouch of Douglas containing small bowel into vaginal lumen. Management: Medical(Kegal, estrogen replacement in postmenopausal, pessaries) surgical(vaginal hysterectomy, anterior/posterior colporrhaphy) Follow-up: walk immediately postoperative period but avoid strenuous activity for 3 months.

Urinary Incontinence
Sensory Irritative In
Etiology History Loss of urine Pelvic exam Neuro exam Ur & culture Cystometric Treatment Infection, stone, tumor, foreign body Urgency, frequency and dysuria. Day or night Suprapubic tenderness n Bacteria, WBC, RBC Unnecessary, n Antibiotics, cystoscopy

Genuine stress
intra-abdominal pressure Coughing & sneezing Not at night/sleep Cystocele, Q tip + n n n Kegal, estrogen replacement, urethropexy

Motor Urge/hypertonic
Involuntary detrusor muscle contraction Large amount of urine loss and urgency Day & night n n n Involuntary detrusor contraction NSAID, Anticholinergics (oxybutynin), Tricyclic Antidepressant, CCB

Overflow/Hypotonic In.
Denervated bladder, medications Intermittent loss in small amount & pelvic fullness Day & night n pudendal nerve sensation May show infection Markedly residual volume Self-catheterization, cholinergics, adrenergic blockers

Bypass Fistula In.

Radical pelvic surgery, pelvic radiation Continuous loss of urine in small amounts Day & night n n n IVP: dye leakage into vagina Surgical repair

Pharmacology of Incontinence
Inhibit Voiding Bladder Relaxants: Antispasmodics: Oxybutynin (Ditropan), Flavoxate (Urispas) Anticholinergics: Oxybutynin (Ditropan), Propantheline (Pro-Banthine) Tricyclic Antidepressants: Imipramine (Tofranil) Vesicle Neck Contraction: Alpha Adrenergics: Ephedrine, Imipramine (Tofranil), Estrogen Vaginal Discharge Etiology Risk Factors Symptoms Speculum Exam Inflammation Sign pH Wet Mount/Micro Treatment Physiologic Discharge Estrogen dominance, Chronic anovulation(PCOS) watery vaginal discharge Thin watery discharge no <4.5 normal normal Steroid contraception with progestine Promote Voiding Bladder Contractors: Cholinergics: Bethanechol (Urocholine), Neostigmine (Prostigmine)

Vesicle Neck Relaxant: Alpha Antagonists: Methyl Dopa, Phenothiazines Trichomonas Vaginitis Flagellated pear shaped pr STD-resides in male semen Itching,burning,dyspareunia Frothy green Strawberry appearance >5 Trichomonads, WBC Oral metronidazole for patient & partner Candida/yeast vaginitis Candida Albicans, not STD Diabetes, antibioics, pregn Itching,burning,dyspareunia Curdy white Edematous & inflamed <4.5 Pseudohyphae, WBC Single oral dose fluconazole or vaginal Azole cream

Bacterial Vaginosis Lactobacilli replaced by bacteria estrogen (postmenop) Fishy odor Thin grayish white, whiff test + no >5 Clue cells, WBC rare Oral/vaginal metronidazole or clindamycin

Vulvar Diseases
Vulvar Lesion with Pruritus/Neoplasia: Most common symptom of both benign & malignant lesions is vulvar itching. Vulvar Dystrophy: Squamous Hyperplasia: white focal/diffuse area, firm & cartilaginous. Treat with fluorinated corticosteroid cream Lichen Sclerosis: bluish white papula, thin & parchment like. Treat with Clobetasol cream Premalignant Vulvar Lesions: Squamous Dysplasia: white, red or pigmented multifocal lesion. Management is surgical excision. CIS: similar to vulvar dysplasia. Management is laser vaporization. Malignant Vulvar Lesions: Squamous Cell: common type of invasive vulvar cancer associated with HPV. Common stage ate diagnosis is Stage 1. Melanoma: any dark or black lesion in vulva. Paget Disease: any red lesion in postmenopausal white woman, associated with cancer of GI tract, GU system & breasts. Diagnosis: Biopsy Staging: surgical Stage 0: CIS, intact basement membrane Stage 1: tumor confined to vulva, 2cm, no palpable nodes (Ia. Invasion 1mm deep, Ib. Invasion >1mm deep) Stage II: tumor confined to vulva, >2cm, no palpable nodes Stage III: spread to lower urethra, vagina or anus; unilateral nodes Stage IV: widespread metastases. (IVa. upper urethra, bladder, rectum, pelvic bone, bilateral nodes; IVb. distant metastasis) Management: Radical vulvectomy and bilateral groin lymphadenectomy of SCC. Complication is Sexual dysfunction. Modified radical vulvectomy: wide local excision for unilateral labial lesions that do not cross midline. Less sexual morbidity. Lymphadenectomy: inguinal node dissection if invasion >1mm (bilateral if midline and unilateral selectively). Lower extremity edema.

Benign Vulvar Lesions

Mulluscom Contagiosum: viral skin infection, STD, umblicated tumor. Management: observation, curettage & cryotherapy Condylomata Acuminata: cauliflower-like vulvar lesions due to HPV type 6 & 11. Treat clinical lesions only. Bartholine Cyst: after infection. ????

Cervical Lesions
Cervical Polyps: Associated with chronic inflammation, abnormal response to increased levels of estrogen or thrombosed cervical blood vessels. Clinic: vaginal bleeding, often after intercourse. Common in older multiparous women. Speculum Exam: smooth fragile red/purple fingerlike projections from cervical canal. Biopsy: mildly atypical cells and signs of infection. Management: Removal by gentle twisting or tying surgical string around base. Base is removed by electrocautery or laser. Antibiotics also given. Nabothian Cysts: seen in women of reproductive age, asymptomatic and do not pose risk to health. Pelvic Exam: small, smooth, rounded lump or collection of lumps on surface of cervix. Or sustained bleeding easily induced by passing cotton swab. Treatment: not necessary. Easily cured with electrocautery or cryotherapy. Cervicitis: mucopurulent cervical discharge is the only symptom. Cervical culture is positive for chlamydia or gonorrhea. Management: oral Azithromycin single dose or oral doxycycline BID for 7d. Cervical Neoplasia Premalignant lesions of cervix are asymptomatic and takes 8-10y to progress to invasive cancer. Common itiology of cervical cancer is HPV 16, 18, 31, 33 and 35. HPV 6 & 11 are associated with benign condyloma acuminate. Risk Factors: early age of intercourse, multiple partners, smoking and immunosuppression. Pap Smear Screening: start at 3y after onset of sexual activity or age 21y, whichever comes first. If <30y old, screen annually with conventional method or every 2y with liquid based method. If 30y, screen every 2-3y. End at age 70y if patient had 3 consecutive normal Pap smears. Pap Smear Classification: ASC (Atypical Squamous Cells): ASC-US (undetermined significance) or ASC-H (can not exclude HSIL) LSIL (low grade squamous intraepithelial lesion): biopsy will demonstrate histologic finding of HPV, mild dysplasia or CIN 1. HSIL (high grade squamous intraepithelial lesion): // moderate-severe dysplasia, CIS, CIN 2 or CIN 3. Cancer ACSUS Pap Smear: If +ACSUS Pap Smear, repeat cytology (Pap smear) in 3-6m OR perform HPV DNA testing in 3m. If it is HPV 6/11 then repeat Pap Smear in 1y. If it is HPV DNA 16/18 then evaluate with colposcopy & biopsy. If follow up is uncertain, directly do colposcopy & biopsy. Etiology: ACSUS Pap smears can result from inflammatory or atrophic lesions, initial stage of HPV infection, premalignant lesion or even cancer. ASCH/LSIL/HSIL/CA Pap Smear: directly go for colposcopy and biopsy. Management According to Histology: CIN 1: no treatment, repeat Pap in 6 & 12m; OR colposcopy & repeat Pap in 12m; OR HPV DNA testing in 12m CIN1, 2, 3: ablative modalities (cryotherapy, laser vaporization, electrofulguration) OR Excision by LEEP or cold knife conization. Biopsy confirmed Recurrent CIN 2, 3: Hysterectomy Follow up: Patients treated with ablative or excisional procedures require repeat Pap OR colposcopy & Pap OR HPV DNA test every 4-6m for 2y.

Invasive Cervical Cancer: Cervical neoplasia that has penetrated through basement membrane. Mean age at diagnosis is 45y.
Presentation: postcoital vaginal bleeding, irregular vaginal bleeding and in advance stage, lower extremity pain & edema. Diagnosis: Cervical biopsy: initial diagnostic test which is most commonly SCC Metastatic Workup: after diagnosis: pelvic exam, CXR, IVP, cystoscopy and sigmoidoscopy Imagimg: ICC is the only gynecologic cancer staged clinically; abdominal pelvic CT or MRI can NOT be used for clinical staging. Staging: is clinical based on pelvic exam and may include IVP: Stage I: only cervix (common stage at diagnosis): Ia1 (invasion 3mm/minimally invasive) Ia2 (microinvasion) Ib (>5mm/frank invasion) Stage II: spread adjacent to cervix: IIa (upper 2/3 of vagina) IIb (parametria) Stage III: spread further from cervix: IIIa (lower 1/3 of vagina) IIIb (extends to pelvic side wall or hydronephrosis Stage IV: Spread furthest from cervix: Iva (bladder or rectum or beyond true pelvis) IVb (distant metastasis) Management: Ia1: simple hysterectomy Ia2: modified radical hysterectomy Ib or IIa: radical hysterectomy +pelvic & paraaortic lymphadenectomy (if premenop), peritoneal washing OR pelvic radiation (if postmen) IIb, III, IV, Metastasis to lymph nodes, >4mm, poorly differentiated lesions or positive margins: radiation & chemotherapy (cis-platinum) Follow up: Pap smear every 3m for 2y after treatment and then every 6m for subsequent 3y. Local recurrence is treated with radiation, if has received radiation previously, consider pelvic exenteration.

Cervical Neoplasia in Pregnancy: Pregnancy does not predispose nor accelerate progression to invasive carcinoma. Abnormal
Pap smear in pregnant is followed same as nonpregnant colposcopy with acetic acid. DO NOT perform ECC (Endocervical Curettage)
Management: CIN: Pap-smear & colposcopy every 3m during pregnancy. At 6-8w postpartum, reevaluate with repeat Pap smear & colposcopy. Treat if + Microinvasion: cone biopsy to ensure no frank invasion. If + for microinvasion carcinoma during pregnancy, follow conservatively, deliver vaginally, reevaluate and treat 2m postpartum. Invasive Carcinoma: if punch biopsy of cervix reveals frank invasive carcinoma, treat according to gestational age: If diagnosed before 24w, do definitive treatment (radical hysterectomy or radiation therapy). If diagnosed after 24w, manage conservatively upto 32-33w to allow for fetal maturity, and perform C-section and begin definitive therapy.

Prevention of Cervical Dysplasia by Vaccination

The quadrivalent HPV recombinant vaccine (Gardasil) is recommended for all females 8-26y of age, with target age of 11-12y. It protects against four HPV types (6, 11, 16, 18) that cause 70% of cervical cancer and 90% of genital warts. 3 doses given, initial, 2m later and 6m later. Testing for HPV is not recommended before vaccination because no easy methods of identifying all types of HPV is available. Continue regular Pap smear guidelines because it does not prevent against all HPV types. Sexually active women, women with previous abnormal cervical cytology or genital warts OR women with previous CIN, all can receive vaccination but benefit is limited. Vaccine is not recommended for pregnant, lactating or immunosuppressed women.

Mullerian Anomalies
Hypoplasia/Agenesis: lack of vagina, cervix, fallopian tubes OR entire body of vagina (except for fundus), also urinary tract anomaly Unicornuate Uterus: one mullarian duct fails to form, a single-horn (banana-shaped) uterus develops. It may have no cavity or have a small space but no opening to vagina. In latter, girl may have monthly pain during adolescence because there is no outlet for menses Didelphys Uterus: Failure of two mullarian dusts to fuse together will result in double uterus. They may share a cervix or have separate cervix each. In 67% cases, a didelphys uterus has 2 vaginas separated by a thin wall. Preterm delivery is common. Bicornuate Uterus: Common uterine anomaly. Failure of fusion between 2 mullarian ducts at top. (stage 1) This failure may be complete, which results in 2 separate uterine bodies sharing 1 cervix. In a partial bicornuate uterus, fusion fails at bottom, resulting in a single uterine cavity at bottom with single cervix, but branches into two hornes at the top. Preterm delivery & malpresentation. Septate Uterus: two mullarian ducts fuse but median septum fail to degenerate (stage 2-3). If failure was complete, median septum persists in entire uterus, separating the uterine cavity into 2 single horned uteri that share one cervix. If failure was partial, result is a single cervix & uterine cavity at bottom, but two distinct horns at top. External shape of uterus is normal single unit shape. //
Arcuate Uterus: normal shape with small midline indentation in fundus. No negative effects on pregnancy. DES Uterus: Dauthers of mothers exposed to diethylstilbestrol during pregnancy are predisposed to uterine anomalies. 2/3 have hypoplastic uterus (small, incompletely formed) or T-shaped cavity. 50% have cervical defects like incompletely formed cervix that predispose to cervical insufficiency. Menorrhagia: heavy menses Metrorrhagia: irregular bleeding in between menses Menometrorrhagia: both heavy menses and bleeding in between menses. Menopause: after 3 continuous months of cessation of menses & elevated gonadotropins. Usually at 52 age

Enlarged Uterus
Adenomyosis: ectopic endometrial glands and stroma are located within myometrium. Commonly diffuse involvement. Mostly asymptomatic but
common symptoms are secondary dysmenorrhea and menorrhagia. (focal involvement surrounded by pseudocapsule = Adenomyoma) Diagnosis: clinical by finding enlarged, symmetric, tender uterus in pelvic exam in absence of pregnancy. Uterus is globular and 2-3 times normal size. Tenderness is common immediately before and during menses. U/S or MRI shows diffusely enlarged uterus with cystic area found within myometrial wall. Histology is the definitive diagnosis. Management: Medical: levonorgestrel (LNG), intrauterine system (IUS) to decrease bleeding. Hysterectomy is definitive treatment.

Leiomyoma Uteri:
benign smooth muscle growth of myometrium. Common in black women. Following locations: Intramural: common location. Within wall of uterus. When small its asymptomatic and cannot be felt in exam. Submucosal: located beneath endometrium and can distort uterine cavity. Abnormal vaginal bleeding with anemia is common Subserosal: located beneath uterine serosa. As tgey grow, they distort external contour causing firm, nontender asymmetry. Depending on their location, they may put pressure on bladder, rectum or ureters. History: size depends on reproductive life stage: Slow Growth: most are small, grow slowly and cause no symptoms. Only when massive in size, do they cause pelvic pressure symptoms. Rapid growth: during times of high estrogen levels, like pregnancy. Degeneration: red/carneous degeneration results in extreme acute pain. This is common during pregnancy. Shrinkage: after menopause or GnRH analog therapy (FSH) Diagnosis: Pelvic exam: enlarged, asymmetric, nontender uterus in absence of pregnancy. Size of fibroid is compared with size of pregnant woman. U/S: abdominal/vaginal U/S will show intramural/subserosal myomas. Saline infusion U/S for submucosal myomas. Hysteroscopy: submucosal myoma Histology: definitive diagnosis Management: Observation: manage conservatively and follow regular pelvic exam Presurgical Shrinkage: 3-6m of GnRH analog therapy (leuprolide or Lupron) will decrease size and decrease blood loss in myomectomy. Or will help perform vaginal hysterectomy rather than abdominal one. (once Lupron stopped, regrowth of fibroid within 6m) Myomectomy: (laparotomy/laparoscopy) to preserve fertility. If incision entered endometrium, delivery of next pregnancy by C-section. Embolization: invasive radiology procedure where catheter is placed in vessel supplying myoma. Microspheres injected cause necrosis. Hysterectomy: definitive therapy (TAH/TVH)

Endometrial Neoplasia/Postmenopausal Bleeding: Common gynecologic malignancy, mean age of diagnosis is 61y.
D/Dx of postmenopausal bleeding: endometrial carcinoma, vaginal/endometrial atrophy, postmenopausal hormonal replacement therapy. Risk Factors: obesity, HTN and diabetes. Others are nulliparity, late menopause and chronic anovulation such as PCO disease. Diagnosis: Endometrial Sampling: postmenopausal bleeding is evaluated with ES. Sometimes cervical stenosis is present which requires dilation & curettage. Hysteroscopy & ultrasonography: with hysteroscopy, cervical/endometrial polyps are identified as cause of postmenopausal bleeding. U/S measures thickness of endometrial lining (normal is <5mm in postmenopausal women) Staging: staging is surgical. Done after pathology evaluation. Stage I: Limited to uterus (common stage at diagnosis):Ia (endometrium), Ib (invasion to < half of myometrium), Ic (> half of myometrium) Stage II: extension to cervix: IIa (only endocervical glands), IIb (invasion to cervical stroma) Stage III: Spread adjacent to uterus: IIIa (invasion to serosa/adnexa/+cytology), IIIb (vagina), IIIc (pelvic/para-aortic nodules) Stage IV: spread further from uterus: Iva (involves bladder or rectum), IVb (distant metastasis) Management: Negative Histology: if ES reveals atrophy and no cancer, treat with estrogen AND progestron replacement. Estrogen alone risk of cancer Positive Histology: If ES reveals adenocarcinoma, treat surgically: Surgical therapy: Total abdominal Hysterectomy (TAH) & bilateral salpingo-oophorectomy (BSO), pelvic & para-aortic lymphadenectomy and peritoneal washings Radiation Therapy: postoperative pathology report will classify prognosis category. Poor prognosis (metastasis to lymph nodes, >50% myometrial invasion, positive surgical margins or poorly differentiated histology) require radiation therapy. Chemotherapy: progestin and cytotoxic agents for metastatic diseases. Prevention: Postmenopausal women taking estrogen replacement therapy and reproductive age women with chronic anovulation such as PCOS must also be treated with progestins to prevent unopposed estrogen stimulation, which may lead to endometrial cancer.

Disorders of Ovary & Oviducts

Functional Ovarian Cyst: Common cause of a simple cystic mass in reproductive age years is a luteal or follicular cyst.
D/Dx: pregnancy, complex adnexal mass (commonly dermoid cyst/benign cystic teratoma; others are endometrioma, tuboovarian abscess/cancer) Diagnosis: negative hCG test and sonogram showing fluid-filled ovarian simple cyst. Management: Follow-up exam in 6-8w (cyst should spontaneously resolve). Alert patient about possibility of acute onset of pain (due to torsion). Oral contraceptive pills prevent further cyst formation. Laparoscopy evaluation is performed if: >7cm or with prior use of steroid contraception 2m. PCOS: Bilateral enlarged ovaries with multiple peripheral cysts (20-100 in each ovary). This is due to high circulating androgens & insulin levels causing arrest of follicular development. This along with stromal hyperplasia & thickened ovarian capsule results in enlarged ovaries. PCOS is associated with valporic acid and is only occur during reproductive years. Patient has severe hirsutism, amenorrhea or irregular anovulatory cycles. Management: Treatment of choice is combination OCP. Metformin will lower insulin resistance and testosterone levels. Ovarian Hyperthecosis: nests of luteinized theca cells scattered throughout stroma of ovary with greater production of androgens and increased production of peripheral estrogen. As a result, risk of endometrial hyperplasia & carcinoma increases, especially in postmenopausal. Severe hirsutism & virilization in postmenopausal are often due to ovarian hyperthecosis than to virilizing ovarian tumor. History & management as PCOS Luteoma of Pregnancy: rare, non-neoplastic tumor like mass of ovary that emerges during pregnancy and regresses spontaneously after delivery. It is usually asymptomatic and is found incidentally during a C-section or postpartum tubal ligation. It can be hormonally active and produce androgens resulting in maternal & fetal hirsutism and virilization. Theca Lutein Cysts: Benign neoplasms stimulated by high levels of FSH and -hCG. They are associated with twins and molar pregnancy but they are rarely associated with normal singleton pregnancy. They regress spontaneously postpartum and require only conservative management.

Prepubertal Pelvic Mass (Germ Cell Tumor): Sudden onset of acute abdominal pain and U/S showing a complex adnexal mass in a teenage girl
is mostly Germ Cell Tumor of ovary. It grows rapidly and gives symptoms early. Dysgerminoma is x-ray sensitive. D/Dx: Follow serum tumor markers: LDH for dysgerminoma, -hCG for choriocarcinoma & -fetoprotein for endometrial sinus tumor. Diagnosis: If U/S shows simple cyst, evaluate with laparoscopy, if it shows complex mass, laparotomy/laparoscopy is performed. Management: Benign Histology: Perform cystectomy instead of salpingo-oophorectomy to conserve both ovaries. If pathology is benign, no further surgery is needed. Follow-up annually. Germ cell tumor: Perform unilateral salpingo-oophorectomy and surgical staging (peritoneal & diaphragmatic biopsy, peritoneal cytology, pelvic & para-aortic lymphadenectomy & omentectomy). Postoperative chemotherapy with vinblastine, bleomycin and cisplatin. Follow up after surgery is every 3m with pelvic exam and tumor marker measurements.

Premenopausal Pelvic Mass (dermoid cyst or benign cystic teratoma)

Commonly complex adnexal mass in young women is dermoid cyst or benign cystic teratoma. OR endometrioma, tubo-ovarian abscess or cancer. D/Dx: pregnancy and functional cysts Diagnosis: negative hCG test and sonogram showing complex mass. Management: surgical Cystectomy: to preserve ovarian function. Evaluate opposite adnexa as dermoid cysts can occur bilaterally in 10% cases. Oophorectomy: if ovarian cystectomy cannot be done due to size of dermoid cyst

Painful Adnexal Mass: Sudden onset of acute unilateral lower abdominal pain in presence of 12cm adnexal mass is presumed as ovarian torsion.
Management: untwist ovary and observe it for few minutes in OR to assure revitalization. This can be performed by laparoscopy or laparotomy. Cystectomy: if revitalization occurs, perform cystectomy to preserve ovary Oophorectomy: if ovary is nercotic, perform unilateral salpingo-oophorectomy Follow up: routine examination 4w after operation and then seen annually.

Postmenopausal Pelvic Mass (Ovarian Cancer): Enlarged ovaries in postmenopausal is suspected for ovarian cancer (age at diagnosis is 69).
DDx: GI tract lesions like diverticular disease (Abdominal pelvic CT/pelvic U/S, GI studies), urinary tract lesions (IVP) Risk Factors: BRCA1 gene, positive family history, high number of lifetime ovulation, infertility and use of perineal talc powder. Protective Factors: OCP, chronic anovulation, breast-feeding and short reproductive life. Screening Test: bimanual pelvic exam is current screening test for ovarian cancer. Pelvic U/S is excellent for finding pelvic masses. Laparotomy 3% Classification of Ovarian Cancer: Epithelial Tumors 80%: predominantly in postmenopausal, they include serous, mucinous, Brenner, endometrioid & clear cell tumor. Germ Cell Tumor 15%: predominantly in teenagers, they include dysgerminoma, endometrial sinus tumor, teratoma, choriocarcinoma. Stromal Tumors 5%: granulosa-theca cell tumors (secrete estrogen & cause bleeding), Sertoli-Leydig cell tumor (secrete testosterone & cause masculinization syndromes). Treat with removal of adnexa (keep fertility) OR TAH & BSO. Metastatic Tumor: common source is endometrium (postmenopausal bleeding+bilateral pelvic mass+enlarged uterus), GI tract & breasts. Krukenberg tumor is mucin-producing tumor from stomach metastatic to ovary. Tumor Markers: CA-125 (cancer antigen 125) & CEA (carcinoembryonic Ag): for possibility of ovarian epithelial cancer (serous carcinoma) LDH, hCG & -fetoprotein: for possibility of germ cell tumors Estrogen & Testosterone: possibility of stromal tumors. Staging: surgical Stage I: limited to ovaries: Ia (1 ovary, intact capsule, -- cytology), Ib (both ovaries, intact capsule, -- cytology), Ic (1/2 ovaries, ruptured capsules, + cytology) Stage II: extension to pelvis: IIa (uterus or tubes), IIb (other pelvic structures), IIc (extension to pelvis & positive cytology) Stage III: Peritoneal metastasis or positive nodes, common stage at diagnosis: IIIa (microscopic peritoneal metastasis), IIIb (Macroscopic peritoneal metastasis 2cm), IIIc (Macroscopic peritoneal metastasis > 2cm) Stage IV: distant metastasis: Iva (bladder or rectum), IVb (distant metastasis) Management: Abdominal pelvic CT done to rule out ascites and spread to abdominal cavity. If negative, laparoscopic evaluation is done. Benign Histology: If patient is not good surgical candidate or desires to maintain fertility unilateral SO. If USO by frozen section is benign and patient is good candidae TAH & BSO even though it was benign. Malignant Histology: cytoreduction (TAH & BSO, omentectomy, bowel resection) and Postop chemotherapy (carboplatin & Taxol) Borderline Cancer (no invasion of basement membrane): if patient desires fertility with unilateral borderline cancer, treat with USO. Otherwise, TAH & BSO is more acceptable. Follow up: if final pathology report was benign, examine annually. If carcinoma, follow up every 3m for first 2y and then every 6m for next 2y with follow-up of CA-125 tumor marker.

Adnexal Mass with Ascites (ovarian carcinoma with Peritoneal Metastasis)

Performan abdominal pelvic CT. Most common ovarian carcinoma spread is by peritoneal disseminatiuon (exfoliation) and commonly metastasizes to omentum and GI tract. Cause of death in advanced ovarian carcinoma is bowel obstruction. Management: Surgical Staging: After CT confirms ascites and adnexal mass, an exploratory laparotomy and surgical staging is performed. SA is done and sent for frozen section evaluation. Debulking Surgery: If ovarian carcinoma is confirmed, debulking (cytoreductive) surgery is performed. Chemotherapy: 6 courses with carboplatin & Taxol and then follow with tumor marker CA-125.

Gestational Trophoblastic Neoplasia/ Molar Pregnancy

Abnormal proliferation of placental tissue involving cytotrophoblast and/or syncytiotrophoblast. It can be benign or malignant. Benign GTN: classic hydatidiform mole: o Complete mole: fertilization of empty egg with single X sperm resulting in paternally derived normal 46, XX karyotype. No fetus, umbilical cord or amniotic fluid seen. Uterus is filled with grape-like vesicles composed of edematous avascular villi. Malignancy 20%. o Incomplete mole results from fertilization of normal egg with 2 sperm resulting in triploid 69, XXY (nonviable fetus). Malignancy 10%. Malignant GTN: this is gestational trophoblastic tumor (GTT) which develops in 3 categories: o Non-metastatic: localized only to uterus. Cure rate is 100%. o Good prognosis metastatic: distant metastasis to pelvis or lung. Cure rate is >95%. o Poor prognosis metastatic: metastasis to brain/ liver, HCG>4000, >4m from antecedent pregnancy, after term pregnancy. Cure 65% Risk Factors: Taiwan & Pilipino women, maternal age extremes (<20y old, >35y old) and folate deficiency. Clinical Findings: bleeding prior to 16w gestation & passage of vesicles from vagina. HTN, hyperthyroidism, hyperemesis gravidarum, proteinuria, no fetal heart tones, fundus larger than dates and bilateral cystic enlargement of ovary (theca-lutein cysts). Diagnosis: Snowstorm ultrasound showing homogenous intrauterine echoes without a gestational sac or fetal parts. Management: Obtain baseline hCG, CXR (rule out lung metastasis), suction D&C (evacuate content) & oral contraceptive (prevent confusion) Benign GTN: weekly serial hCG until for 3w, then monthly until negative for 12m. Follow up for 1y. if titers plateau or rise, patient diagnosed with persistent gestational trophoblastic disease and undergo metastatic workup (CT of brain, thorax, abdomen & pelvis) . Non-metastatic/ Good Prognosis metastatic: single agent (methotrexate/actinomycin D) till weekly hCG for 3w, monthly until for 12m Poor Prognosis Metastatic: Metotrexate+Actinomycin D+Cytoxan until weekly hCG for 3w, then monthly titer for 2y, every 3m for 3y.

PID: Spectrum of upper genital tract conditions. Most common initial organisms are chlamydia and gonorrhea. Pathophysiology:
PID
sym

Cervicitis: initial infection starts with invasion of cervix with chlamydea and gonorrhea. Acute Salpingo-oophoritis: usually after a menstrual period with breakdown of cervical mucus barrier, pathologic organisms ascend and enter oviducts without casing endometritis. Chronic PID: if above not treated well, bodys immune will overcome the infection but leave persistent adhesions & scarring. Tubo-ovarian Abscess: develops when bodys immune defense cannot overcome infection. Cervicitis
Vaginal discharge Cervical discharge

ASO
Bilateral pelvic pain, gradual/sudden onset, often after menses, nausea & vomiting Cervical discharge, cervical motion & bilateral adnexal tenderness, fever, tachycardia, peritoneal signs & guarding WBC & ESR, laparoscopy shows inflammatory sign on oviducts, +cervical culture for chlamydia & gonorrhea Adnexal tortion, ectopic pregnancy, endometriosis, appendicitis, diverticulitis, CD, UC clinical Outpatient: if certain diagnosis, no fever or pelvic abscess: ofloxacin bid+metronidazole bid for 14d Inpatient: if uncertain diagnosis, pelvic abscess, nulligravida, adolescence, IUD in place outpatient treatment failure, f >39C: IV cefoxitin/cefotetan + IV doxycycline OR IV clindamycin + gentamicin

TOA
Septic appearance, severe pelvic , back & rectal pain, painful bowel movement, nausea & vomiting Gravely sick looking, fever, tachycardia, peritoneal signs & guarding, palpable mass, painful pelvic exam WBC ESR +cervical culture for chlamydia & gonorrhea, +blood cultures for gram - & bacteroides fragilis. Culdocentesis yield pus. U/S & CT bilateral complex pelvic mass Adnexal tortion, Septic abortion, diverticular abscess, appendiceal abscess, Inpatient IV clindamycin + gentamicin (72h) If no response/rapture of abscess: Exploratory laparotomy with possible TAH & BSO OR Percutaneous drainage through colpotomy incision

Chronic PID
Chronic pelvic pain, infertility, dyspareunia, history of ectopic pregnancy and vaginal bleeding. Bilateral adnexal tenderness and cervical motion tenderness. No discharge, fever or tachycardia Normal WBC & ESR, -- cultures. U/S shows bilateral cystic pelvic mass consistent with hydrosalpinges.

exam

Lab

???

DDx
Dx Treat lab Single dose oral cefixime & azithromycin

Laparoscopy : pelvic adhesion Outpatient mild analgesics. Lysis of tubal adhesion will help fertility. Severe unremitting pelvic pain require TAH & BSO If ovaries removed: estrogen replacement therapy is indicated.

Primary Dysmenorrhea: recurrent, cramp lower abdominal pain with nausea, vomiting & diarrhea that occur during menses in absence of
pelvic pathology. Common in adolescents, symptoms start several hours prior to onset of menses and continue for 1-3d. Management: NSAID is first choice and continuous combination OCP is second choice.

Secondary Dysmenorrhea: Endometriosis, adenomyosis and ectopic pregnancy

Endometriosis: endometrial glands & stroma are outside uterus resulting in retrograde menstruation (Sampson Theory). 1 common site is ovary, nd which bleeds monthly and creates adnexal enlargement known as endometriomas or chocolate cyst. 2 most common site is cul-de-sac, with uterosacral ligament nodularity, tenderness in rectovaginal exam, fixed retroverted uterus, dyspareunia & painful bowel movements (dyschezia). Diagnosis: CA-125, endometrioma on U/S but definitive Dx is laparoscopic identification of endometrial nodules or endometriomas. Medical Management: Pregnancy: will help atrophy of ectopic endometrium, however infertility is common in endometriosis Psudopregnancy: by continuous oral MPA (Provera), IM DMPA (Depo Provera) or combination OCP Pseudomenopause: by testosterone derivative (Danocrine/Danazol) or GnRH analog (leuprolide or Lupron) for 3-6m (during which patient will complain of menopausal symptoms) and then alternate Lupron with DMPA (Depo Provera) Surgical Management: Conservative to preserve fertility: laparoscopic lysis of paratubal adhesions & laser vaporization of visible lesions. Ovarian cystectomy & oophorectomy for endometriomas Aggressive if severe pain & fertility not desired: TAH & BSO followed with estrogen replacement therapy.

st

Menstrual Abnormalities
Premenarchal Vaginal Bleeding: average age at menarche is 12y old.
DDx & Etiology: ingestion of estrogen medication, foreign body irritating vaginal lining, cancer of vagina or cervix (sarcoma botryoides), tumor of pituitary or adrenal gland, ovarian tumor, sexual abuse or idiopathic precocious puberty. Dx & Management: Pelvic exam under sedation: look for forigne body, sexual abuse or sarcoma botryoides (like grapes arising from vagina or cervix) CT/MRI of pituitary, abdomine and pelvic: look for pituitary, adrenal or ovarian tumor that causes early estrogen production.

Abnormal Vaginal Bleeding: irregular bleeding during reproductive age

DDx, Dx & Management: Pregnancy or its complications: -hCG test & pelvic U/S. Treat according diagnosis. Anatomic lesions like vaginal lesions (laceration, tumors), cervical lesions (polyps, cervicitis, tumors), endometrial lesions (submucous leiomyomas, polyps, hyperplasia, cancer) or myometrial lesions (adenomyosis): pelvic exam, saline U/S, endometrial sampling & hysteroscopy. Treat according diagnosis. Dysfunctional Uterine Bleeding (anovulation): this bleeding is without cramping, cervical mucus is clear, thin & watery. No midcycle temperature rise in basal body temperature chart. Endometrial biopsy will show proliferative endometrium. Identify correctable causes of anovulation like hypothyroidism or hyperprolactinemia by a TSH & prolactin level. Treat DUB either with cyclic progestin therapy from day 14 to 25 of each cycle OR with daily combination OCP. Cases that fail hormonal therapy are managed by either endometrial ablation (using microwave or thermal methods) or hysterectomy. Primary Amenorrhea: absence of menses at age 14 without secondary sexual development OR age 16 with secondary sexual development. Management: first see if breast are present or absent? Is uterus present or absent? (by U/S) Both Present: imperforate hymen, vaginal septum, anorexia nervosa, excessive exercise & possibility of pregnancy before first menses. History & physical exam will diagnose above causes otherwise proceed as if for secondary amenorrhea. Breasts present, uterus absent: testosterone levels & karyotype will diagnose the following: o Mullerian agenesis (Rokitansky-Kuster-Hauser syndrome): genetically normal females (46, XX) with idiopathic absence of fallopian tubes, uterus, cervix and upper vagina. Secondary sexual characteristics, normal pubic and axillary hair are present because ovaries are present. Testosterone levels are normal female. Management: Surgically elongate vagina for satisfactory intercourse. IVF-surrogate o Complete androgen insensitivity (testicular feminization): genetically male (46, XY) with female external genitalia. They function psychologically and physically as females and female secondary sexual characteristics are present because testes secret estrogens. No pubic or axillary hair. Testosterone levels are normal male. Management: Remove testes at age 20 because higher temperature associated with intra-abdominal position of testes may lead to testicular cancer. Estrogen replacement is then needed. Create vagina. Breasts absent, uterus present: FSH level & karyotype will diagnose the following: o Gonadal Dysgenesis (Turner Syndrome 45,X): instead of ovaries, streak gonads develop, therefore no estrogen. FSH because of lack of estrogen feedback to hypothalamus & pituitary. No secondary sexual characteristics present. Management: Give estrogen and progesterone replacement o Hypothalamic-pituitary failure: low FSH. Kallman Syndrome (primary amenorrhea, no breasts & ansomia) is inability of hypothalamus to produce GnRH. CNS imaging will rule out brain tumor. Management: estrogen and progesterone replacement Secondary Amenorrhea: absence of menses for 3m if previously regular menses OR for 6m if previously irregular menses. Etiology: Pregnancy Anovulation: initially patient demonstrates amenorrhea but later, irregular, unpredictable bleeding will occur. Causes of anovulation are PCOS, hypothyroidism, pituitary adenoma, prolactin and medications like antipsychotics and antidepressants. Estrogen Deficiency: due to ovarian follicular failure or hypothalamic-pituitary insufficiency. Outflow Tract Obstruction: obliterated endometrial cavity or stenosis of lower reproductive tract. Management: step by step hCG Test: initial test always Thyrotropin (TSH) level: levels (lead to prolactin) indicate hypothyroidism. Treat with thyroid replacement therapy. Prolactin Level: if , check for antipsychotics/antidepressants OR perform Brain CT/MRI for pituitary tumor. If tumor<1cm, bromocriptine (Parlodel), if >1cm treat surgically. If cause of prolactin is idiopathic, treatment is also with bromocriptine (Parlodel). Progestin Challenge Test: if all above negative/normal, give single IM progesterone OR 7d oral medroxy progesterone acetate (MPA). Positive PCT: any degree of withdrawal bleeding is diagnostic for anovulation. Cyclic MPA is required to prevent endometrial hyperplasia. Clomiphene ovulation induction is required if pregnancy is desired. Estrogen-Progesterone Challenge Test: if PCT negative, give 21d of oral estrogen followed by 7d of MPA. Positive EPCT: any degree of withdrawal bleeding is diagnostic of inadequate estrogen. An FSH level will identify itiology: o FSH suggests ovarian failure. If this occurs before age 25y, it could be due to Y chromosome mosaicism associated with maliganancy, so order a karyotype. Savage Syndrome/resistant ovary syndrome (follicles seen by U/S but do not respond) o FSH suggests hypothalamic-pituitary insufficiency. Order Brain CT/MRI to rule out brain tumor. Whatever the results, +EPCT requires estrogen replacement therapy to prevent osteoporosis and Cyclic progestin to prevent endometrial hyperplasia. Negative EPCS: absence of withdrawal bleeding is diagnostic of outflow tract obstruction OR endometrial scarring (Asherman Syndrome). Hysterosalpingogram will identify lesion. Asherman Syndrome is result if extensive uterine curettage and infection produced adhesions. Treat by hysteroscopic adhesion lysis followed by estrogen stimulation of endometrium. An inflatable stent is then placed into uterine.

Premenstrual Disorders
Symptoms include fluid retention (bloating, edema, breast tendernss), autonomic changes (insomnia, fatigue, herat pounding), emotional symptoms (crying, anxiety, depression, mood swings) or musculskeletal complaints (headache, muscl aches, joint aches. Criteria for Premenstrual Syndrome: all must be present: Recurrent symptoms in at least 3 consecutive cycles Absence of symptoms in preovulatory phase of menses Presence of symptoms in 2 postovulatory weeks Symptoms must interfere with normal functioning Symptoms must resolve with onset of menses. Criteria for Premenstrual Dysphoric Disorder: Presence of 5 of following symtoms most time during last week of luteal phase and abscent in week after menses, in most cycles during past year, with atleast 1 symtom being either 1, 2, 3 or 4: 1. Markedly depressed mood, feeling of hoplessness or self-deprecating thoughts 2. Marked anxiety, tension or feeling on edge 3. Marked affective lability (feeling suddenly sad or tearful) 4. Marked anger or irritability or increased interpersonal conflicts 5. Decreased interest in usual activities 6. Sense of difficulty concentrating 7. Lethargy, easy fatigability or marked lack of energy 8. Marked change in appetite, overeating or specific mood cravings 9. Hypersomnia or insomnia 10. Breast tenderness or swelling, headache, joint or muscle pain, sensation of bloating or weight gain. Disturbance markedly interferes with work or school Disturbance is not merely exacerbation of major depressive disorder, panic disorder, dysthymic disorder or personality disorder First 3 criteria must be confirmed by daily ratings during al least 2 consecutive symptomatic cycles. Management of PMS & PMDD: Balanced diet that is low in sugar, salt and caffeine. Relaxation techniques and regular exercise. Selective Serotonin Reuptake Inhibitor: fluoxetine hydrochloride (Prozac), buspirone Hcl (BuSpar) and meclofenamate sodium are effective for emotional and behavioral symptoms but fluoxetine is treatment of choice for PMS and only fluoxetine, alprazolam and GnRH agonist have proved effective for severe symptoms of PMDD. Yaz (drospirenone/ethinyl estradiol) a combination OCP with unique progestin called drospirinon (DRSP) approved by FDA for PMDD. Spironolactone is also effective for PMS. No not give Pyridoxine and progesterone.

Precocious Puberty: Development of female secondary sexual characteristics & accelerated growth before age 8 in girls and age 9 in boys.
Normal Pubertal Landmarks: Thelarche (breast development at 9-10y), Adrenarche (pubic & axillary hair at 10-11y), Maximam Growth rate occurs between 11 & 12y, Menarche (onset of menses at age 12-13). Incomplete Isosexual Precocious Puberty: it involves only one change, either thelarche, adrenarche, or menarche. It is result of eithrr transient hormonal elevation or unusual end-organ sensitivity. Management is conservative. Complete Isosexual Precocious Puberty: all changes of puberty are seen including breast development, growth spurt and menstrual bleeding. The primary concern is premature closure of distal epiphysis of long bones resulting in short stature. Fertility & sexual response are not impaired. Etiology & management: Idiopathic: 80%constitutional (6/7y). Diagnosis is made when CNS imaging show normal. Treat with GnRH agonist suppression (leuprolide or Lupron) until appropriate maturity or height has been reached. CNS Pathology: age <6y, abnormal CNS imaging, due to hydrocephalus, von Recklinghausen disease, meningitis, sarcoid and encephalitis. McCune-Albright Syndrome (polyostotic fibrous dysplasia): autonomous stimulation of aromatase enzyme production of estrogen by ovaries. It includes precocious puberty 5%, multiple cystic bone lesions & caf au lait skin spots. Give aromatase enzyme inhibitor. Granulosa cell Tumor: gonadal-stromal cell ovarian tumor that produces estrogen. Pelvic mass is identified on pelvic exam and imaging. Management is surgical removal of tumor. Follow up: continue treatment of idiopathic precocious puberty until chronologic age catches up with bone age.

Menopause: 3m of amenorrhea with FSH & LH due to lack of estrogen. Mean age of 51y is genetically determined and NOT by pregnancy or
use of steroid contraception (2y earlier in smokers). Premature Menopause occurs between 30-40y & mostly idiopathic or after radiation therapy or surgical oophorectomy. Premature ovarian failure occurs before 30y and associated with autoimmune disease /Y chromosome mosaicism Clinic: anovulation, then secondary amenorrhea in 3-5y, hot flashes (NOT in obese women-adipose tissue produce estrone), vaginal lubrication, vaginal pH & infection, urinary tract symptoms, mood alteration, sleep disorders, depression, cardiovascular disorders and osteoporosis Hormone Replacement Therapy: common current regimen is oral estrogen & progestin given continuously. Start low dose, NOT for more than 4y (risk of breast cancer). Women without uterus are given continuous estrogen only. The only indication for HT is vasomotor symptoms, NOT prevention of osteoporosis or cardiovascular disorders. Contraindications are estrogen sensitive breast/endometrial cancer, active liver disease, active thrombosis and unexplained vaginal bleeding. Give instead, SERMs which protect against heart & bone but not effective on hot flashes: Tamoxifen (prevents breast cancer but risks endometrial cancer, cataract & DVT) and Raloxifene (prevents osteoporosis and breast cancer, no risk of endometrial cancer). For osteoporosis, SERM (raloxifene) and bisphosphonates are first choices but if not enough, only then estrogen therapy. Osteoporosis is common in trabecular bone type, in vertebral body leading to crush fractures, kyphosis & height. Next, hip & wrist fractures are common. Risk factors are family history in thin white female, steroid use, low Ca intake, smoking and alcohol. For diagnosis, assess bone density with DEXA scan & assess Ca loss with 24h urine hydroxyproline or NTX. For prevention give Ca & vit D, exercise & above medications.

Fertility Control
Barrier Spermicidal Methods: condoms, diaphragm and spermicides (nonoxynol-9) Advantage: effective with advanced age & associated decline in fertility, protection against STD and no systemic side effects. Disadvantage: failure rate 20%, coitally dependent, no impact on painful heavy menses Steroid Contraception: inhibits LH surge & ovulation, endometrium inhibits implantation, thick & viscid cervical mucus inhibits sperm penetration Estrogen Mediated Metabolic Effects: fluid retention from Na excretion, development of cholelithiasis, hepatic protein production (coagulation factor, carrier protein, angiotensinogen), HDL, LDL and thrombosis Progestin Mediated Metabolic Effects: mood changes & depression from serotonin levels, androgenic effects (weight gain , acne), HDL, LDL Absolute Contraindication: pregnancy, acute liver disease, history of vascular disease (thromboembolism, DVT, CVA, SLE), hormonally dependent breast cancer, smoker 35, uncontrolled HTN, migraines with aura, diabetes with vascular disease and known thrombophilia. Relative Contraindication: migraine headache, depression, diabetes mellitus, chronic HTN & hyperlipidemia. Non-contraceptive Benefits: mostly Progestin component: ovarian & endometrial cancer, dysmenorrhea & DUB, PID & ectopic pregnancy.

Combination Modalities:
Combination OCP: contain both estrogen & progestin taken daily with 21d on & 7d off OR daily 24d on & 4d off. They are the only steroid contraceptive with regular predictable menses. Failure rate 2%. A newer combination is daily hormones for 12w followed by 1w of placebo. Oral Contraceptive: YAZ a unique combination OCP has ethynyl estradiol & a new progestin called drospirenone. It reduces severe PMDD symptoms. Taken 24d of active pill followed by 7d of placebo. Combination Vaginal Ring (NuvaRing): inserted into vagina for 3w, removed for 1w to allow withdrawal bleed. Failure rate as comb OCP Transdermal Skin Patch (Ortha Evra): replaced every week for 3w, removed for 1w. 60% higher steroid level than combination OCPs.

Progestin Only Modalities:

Progestin-Only OCP (minipill): taken daily & continuously. Frequent side effect is breakthrough bleeding. Failure rate is 3%. Progestin-Only Injectable (Depo-Provera): IM injection of DMPA every 3m. Frequent side effect is breakthrough bleeding. Failure rate is <1%. Progestin-Only Subcutaneous Implant (Implanon): active ingredient is etonogestrel, every 3y. // Morning After Pill (Plan B): 1 tablet of levonorgestrel taken immediately (within 3d) & followed by another tablet in 12h. Failure rate is 1%.

Intrauterine Contraception
Mechanism of Action: inhibition of sperm transport, tubal motility causing failure of implantation of immature zygote, inhibition of implantation due to endometrial inflammation, destruction of sperm & blastocyst; and change in cervical mucus (only progesterone IUS) . Absolute Contra: confirmed/suspected pregnancy, known/suspected pelvic malignancy, undiagnosed vaginal bleeding,known/suspected salpingitis. Relative Contraindication: abnormal uterine size or shape(leiomyomas, uterine fibroids, NOT subserosal fundal fibroids), corticosteroid therapy, valvular heart disease, immune suppression, nulligravidity, abnormal Pap Smear and history of ectopic pregnancy. Side Effects: menstrual bleeding & pain with copper IUS Complications: expulsion (>young low parity women), ectopic pregnancy, septic abortion with concurrent pregnancy, uterine perforation at time of insertion is rare, PID occur within first 2m after placement if pathogenic organisms are present in reproductive tract. Mirena (levonorgestrel-impregnated/LNG): 5y. bleeding & cramping. Failure rate is <1%. Copper -380A (Paraguard): 10y. bleeding & cramping. Failure rate is <1%.

Sterilization: Permanent and irreversible

Tubal Ligation: Ligation of female oviduct in OR with laparoscope. If it failed & pregnancy occurred, rule out ectopic pregnancy. Vasectomy: ligation of male vas deferens in OPD with local anesthesia. Confirm by absence of sperm on semen collected 12 ejaculations after surgery. Sperm Ab found in 50% of vasectomized patients.

Infertility
Infertility is inability to achieve pregnancy after 12m of unprotected and frequent intercourse. Fecundability is likelihood of conception occurring with one cycle of appropriately timed midcycle intercourse. At age 20, fecundity rate is 20% and at 35, its 10%. Initial Noninvasive Tests Semen Analysis: normal values are volume>2ml, pH 7.2-7.8, sperm density>20million/ml, sperm motility >50% and sperm morphology >50% normal. If abnormal values, repeat in 4-6w. Obtain semen after 2-3d of abstinence and examine within 2h. o If sperm density mild or moderately lower than normal: intrauterine insemination (IUI) is used. o If severe abnormality in semen: intracytoplasmic sperm injection (ICSI) is used in conjunction with IVF & embryo transfer. o No viable sperm: if azoospermia or failed ICSI, artificial insemination by donor (AID) is used. Anovulation: history of irregular, unpredictable menses, minimal or no uterine cramping, no midcycle temperature elevation, serum progesterone, proliferative histology in endometrial biopsy. o if due to hypothyroidism or hyperprolactinemia: treat cause o ovulation induction: oral clomiphene citrate for 5d beginning on day 5 of menses. If clomiphene failed: parental HMG Follow up Invasive Tests: Assessment of fallopian tube abnormalities is next step if semen analysis is normal and ovulation is confirmed. Hysterosalpingogram: scheduled during week after end of menses and after prophylactic antibiotics. o If it shows normal anatomy, no further tests are done. o If abnormal findings seen, note the site of pathology and do laparoscopy. Chlamydia Antibody: a negative IgG Ab test for chlamydia virtually rules out infection including tubal adhesions. Laparoscopy: visualize oviducts and reconstruct if possible (tuboplasty). If tubal damage is severe and surgfical therapy is futile, plan IVF. Unexplained Infertility: diagnosed when semen analysis is normal, ovulation is confirmed and patent oviducts are noted. 60% couples with unexplained infertility will achieve spontaneous pregnancy within next 3y. Manage by controlled ovarian hypersimulation with clomiphene and appropriately timed preovulatory intrauterine insemination. Fecundity rate for 6m are comparable with IVF.

Sexual Dysfunction
Desire Disorders: desire may be organic (low androgens), medication related (SSRI) or psychological (poor partner relationship) Excitement Disorder: estrogen deficiency results in difficulty in vaginal lubrication. Anorgasmia: due to inadequate clitoral stimulation. Treatment: self-stimulation first then partner education Dyspareunia: psychologic or physiologic causes therefore thorough history & physical exam is required. Vaginismus: painful reflex spasm of paravaginal thigh adductor muscles. Diagnosed on physical exam & treated with vaginal dilators.

Sexual Assault
Stabilization: first step is to check vital signs and stabilize them. Ann informed consent I required. History Taking: record the even in patients own words. Also obtain a reproductive, obstetric, sexual & contraceptive history. Examination: general & pelvic exam with photographic or drawing documentation of any injury or trauma Specimen: use rape kit to obtain biologic specimens (vaginal, oral or anal) for DNA or other evidence for use in legal proceedings. Appropriately label & document them, with signatures of receiving authority. Baseline Lab Tests: VDRL, HIV screen, pregnancy test, urine drug screen, blood alcohol level Prophylaxis: antibiotic for gonorrhea (cephalosporin), chlamydia (doxycycline) & trichomonas (metronidazole). Antiviral HIV prophylaxis given within 24h after exposure but no medications given after 36h. Active & passive immunization for HBV. Pregnancy Prevention: give 2 tablets of high progestin OCPs immediately, repeating 2 tablets in 12h.

Hirsutism
Hirsutism is excessive male-pattern hair growth in a woman on upper lip, chin, chest, abdomen, back & proximal extremities. Virilization is excessive male pattern hair growth in a woman plus clitorimegaly, baldness, lowering of voice, muscle mass & loss of female body contours. Adrenal Tumor: Rapid onset virilization, - family history, DHEAS level, abdominal/flank mass in CT/MRI. Treat by surgical removal. Ovarian Tumor: Rapid onset virilization, -family history, adnexal mass on pelvic exam & U/S, testosterone. Treat by surgical removal. Congenital Adrenal Hyperplasia/21-Hydroxyolase Deficiency: gradual onset hirsutism, family history, 17-OH progesterone, anovulation & menstrual irregularities. Precocious puberty with short stature common. Treat: continuous corticosteroid replacement. PCOS: gradual onset hirsutism, +family history, Testosterone, LH, SHBG, infertility & menstrual irregularities, obesity, acne, acanthosis nigricans, bilateral enlarged ovaries with multiple follicles in U/S. Treatment of choice is combination OCP. Metformin decreases insulin resistance and lower testosterone levels. For infertility, clomiphene citrate or human menopausal gonadotropin. Idiopathic: due to 5- Reductase activity in hair follicle with gradual onset hirsutism and +family history. Treatment of choice is spironolactone. Elfornithine (Vaniqa) tropical drug for treatment of unwanted facial & chin hair.