Blueprints Obstetrics And Gynecology 5th Edition PDF

FRONT OF BOOK ↑ [+] Authors - Preface - Acknowledgments [+] Abbreviations TABLE OF CONTENTS ↑ [+] Part 1 - Obstetrics [+] Part 2 - Gynecology BACK OF BOOK ↑ - Questions - Answers [+] Index [+] Color Plates Preface In 1997, the first five b...

FRONT OF BOOK ↑ [+] Authors - Preface - Acknowledgments [+] Abbreviations TABLE OF CONTENTS ↑ [+] Part 1 - Obstetrics [+] Part 2 - Gynecology BACK OF BOOK ↑ - Questions - Answers [+] Index [+] Color Plates Preface In 1997, the first five books in the Blueprints series were published as board review for medical students, interns, and residents who wanted high-yield, accurate clinical content for USMLE Steps 2 and 3. Twelve years later, we are proud to report that the original books and the entire Blueprints brand of review materials have far exceeded our expectations. The feedback we've received from our readers has been tremendously helpful and pivotal in deciding what direction the fifth edition of the core books would take. To ensure that the fifth edition of the series continues to provide the content and approach that made the original Blueprints a success; we have expanded the text to include the most up-to-date topics and evidence-based research and therapies. Information is provided on the latest changes in the management of cervical dysplasia, preeclampsia, cervical insufficiency, and preterm labor. The newest and future techniques in contraception and sterilization and hormone replacement therapies are covered, as are contemporary treatment options for uterine fibroids and invasive breast cancer. The succinct and telegraphic use of tables and figures was highly acclaimed by our readers, so we have redoubled our efforts to expand their usefulness by adding a significant amount of updated and improved artwork including a new section of color plates. In each case, we have tried to include only the most helpful and clear tables and figures to maximize the reader's ability to understand and remember the material. Our readers also asked for an enhanced art program, so a tri-color system is being used in this edition to increase the usefulness of the figures and tables. We have likewise changed our bibliography to include updated evidence-based articles as well as references to classic articles and textbooks in both obstetrics and gynecology. These references are now provided at the end of the book and are further expanded in the on-line references. It was also suggested that the review questions should reflect the current format of the boards. We are particularly proud to include new and revised boardformat questions in this edition with full explanations of both correct and incorrect options provided in the answers. What we've also learned from our readers is that Blueprints is more than just board review for USMLE Steps 2 and 3. Students use the books during their clerkship rotations, subinternships, and as a quick refresher while rotating on various services in early residency. Residents studying for USMLE Step 3 often use the books for reviewing areas that were not their specialty. Students in physician assistant, nurse practitioner, and osteopath programs use Blueprints either as a companion or in lieu of review materials written specifically for their areas. When we first wrote the book, we had just completed medical school and started residency training. Thus, we hope this new edition brings both that original viewpoint as well as our clinical experience garnered over the past 12 years. However you choose to use Blueprints, we hope that you find the books in the series informative and useful. Tamara L. Callahan MD, MPP Aaron B. Caughey MD, MPP, MPH, PhD Abbreviations Abbreviations 3β-HSD 3β-hydroxysteroid dehydrogenase 5-FU 5-fluorouracil 17α-OHP 17α-hydroxyprogesterone ABG arterial blood gas ACTH adrenocorticotropic hormone AD autosomal dominant ADH antidiuretic hormone AED antiepileptic drug AFE amniotic fluid embolus AFI amniotic fluid index AFLP acute fatty liver of pregnancy AFP α-fetoprotein AGUS atypical glandular cells of undetermined significance AIDS acquired immunodeficiency syndrome ALT alanine transaminase AMA advanced maternal age APA antiphospholipid antibody AR autosomal recessive ARDS adult respiratory distress syndrome AROM artificial rupture of membranes ART assisted reproductive technology ASC atypical squamous cells ASC-H atypical squamous cells cannot exclude high-grade squamous intraepithelial lesion ASC-US atypical squamous cells of undetermined significance AST aspartate transaminase AV arteriovenous AZT zidovudine β-hCG beta human chorionic gonadotropin BID twice a day BP blood pressure BPP biophysical profile BUN blood urea nitrogen BV bacterial vaginosis CAH congenital adrenal hyperplasia CBC complete blood count CCCT clomiphene citrate challenge test CF cystic fibrosis CHF congestive heart failure CIN cervical intraepithelial neoplasia CKC cold-knife conization (biopsy) CMV cytomegalovirus CNS central nervous system CPD cephalopelvic disproportion CPK creatine phosphokinase CRS congenital rubella syndrome CSF cerebrospinal fluid CT computed tomography (CAT scan) CVA cerebrovascular accident CVAT costovertebral angle tenderness CVD collagen vascular disorders CVS chorionic villus sampling CXR chest x-ray DA developmental age D&C dilation and curettage D&E dilation and evacuation DCIS ductal carcinoma in situ DES diethylstilbestrol DEXA dual-energy x-ray absorptiometry DHEA dehydroepiandrosterone DHEAS dehydroepiandrosterone sulfate DHT dihydrotestosterone DIC disseminated intravascular coagulation DMPA depot medroxyprogesterone acetate (Depo-Provera) DTRs deep tendon reflexes DUB dysfunctional uterine bleeding DVT deep venous thrombosis ECG electrocardiogram EDC estimated date of confinement EDD estimated date of delivery EFW estimated fetal weight EIF echogenic intracardiac focus ELISA enzyme-linked immunosorbent assay EMB endometrial biopsy EMG electromyography ERT estrogen replacement therapy ESR erythrocyte sedimentation rate FAS fetal alcohol syndrome FH fetal heart FHR fetal heart rate FIGO International Federation of Gynecology and Obstetrics P.xi FIRS fetal immune response syndrome FISH fluorescent in situ hybridization FNA fine-needle aspiration FSE fetal scalp electrode FSH follicle-stimulating hormone FTAABS fluorescent treponemal antibody absorption FTP failure to progress G gravidity GA gestational age GBS group B streptococcus GDM gestational diabetes mellitus GFR glomerular filtration rate GH gestational hypertension GI gastrointestinal GIFT gamete intrafallopian transfer GLT glucose loading test GnRH gonadotropin-releasing hormone GSI genuine stress incontinence GTD gestational trophoblastic disease GTT glucose tolerance test GU genitourinary HAART highly active antiretroviral therapy Hb hemoglobin HbH hemoglobin H disease hCG human chorionic gonadotropin hCS human chorionic somatomammotropin Hct hematocrit HDL high-density lipoprotein HELLP hemolysis, elevated liver enzymes, low platelets HIV human immunodeficiency virus HLA human leukocyte antigen hMG human menopausal gonadotropin HPI history of present illness HPL human placental lactogen HPV human papillomavirus HR heart rate HRT hormone replacement therapy HSG hysterosalpingogram HSIL high-grade squamous intraepithelial lesion HSV herpes simplex virus I&D incision and drainage ICSI intracytoplasmic sperm injection ID/CC identification and chief complaint Ig immunoglobulin IM intramuscular INH isoniazid INR International Normalized Ratio ITP idiopathic thrombocytopenia purpura IUD intrauterine device IUFD intrauterine fetal demise or death IUGR intrauterine growth restricted IUI intrauterine insemination IUP intrauterine pregnancy IUPC intrauterine pressure catheter IUT intrauterine transfusion IVC inferior vena cava IVF in vitro fertilization IVP intravenous pyelogram JVP jugular venous pressure KB Kleihauer-Betke test KOH potassium hydroxide KUB kidneys/ureter/bladder (x-ray) LBW low birth weight LCHAD long-chain hydroxyacyl-CoA dehydrogenase LCIS lobular carcinoma in situ LDH lactate dehydrogenase LDL low-density lipoprotein LEEP loop electrosurgical excision procedure LFT liver function test LGA large for gestational age LGV lymphogranuloma venereum LIQ lower inner quadrant LH luteinizing hormone Lletz large loop excision of the transformation zone LMP last menstrual period LOQ lower outer quadrant LOT left occiput transverse LSIL low-grade squamous intraepithelial lesion LTL laparoscopic tubal ligation Lytes electrolytes MAO monoamine oxidase MESA microsurgical epididymal sperm aspiration MHATP microhemagglutination assay for antibodies to T. pallidum MI myocardial infarction MIF müllerian inhibiting factor MLK myosin light-chain kinase MRI magnetic resonance imaging MRKH Mayer-Rokitansky-Kuster-Hauser (syndrome) MSAFP maternal serum α-fetoprotein MTHFR methyl tetrahydrofolate reductase NPO nil per os (nothing by mouth) NPV negative predictive value NRFT nonreassuring fetal testing NSAID nonsteroidal anti-inflammatory drug NST nonstress test NSVD normal spontaneous vaginal delivery NT nuchal translucency NTD neural tube defect OA occiput anterior OCP oral contraceptive pill P.xii OCT oxytocin challenge test OI ovulation induction OP occiput posterior OT occiput transverse OTC over-the-counter P parity PBS peripheral blood smear PCOD polycystic ovarian disease PCOS polycystic ovarian syndrome PCR polymerase chain reaction PDA patent ductus arteriosus PE physical exam PE pulmonary embolus PET preeclampsia/toxemia PFTs pulmonary function tests PID pelvic inflammatory disease PIH pregnancy-induced hypertension PMDD premenstrual dysphoric disorder PMN polymorphonuclear leukocyte PMOF premature ovarian failure PMS premenstrual syndrome PO per os (by mouth) POCs products of conception POP progesterone-only contraceptive pills Pop-Q pelvic organ prolapse quantification system PPCM peripartum cardiomyopathy PPD purified protein derivative PPROM preterm premature rupture of membranes PPS postpartum sterilization PPV positive predictive value PROM premature rupture of membranes PSTT placental site trophoblastic tumor PT prothrombin time PTL preterm labor PTT partial thromboplastin time PTU propylthiouracil PUBS percutaneous umbilical blood sampling PUS pelvic ultrasound QD each day QID four times a day RBC red blood cell RDS respiratory distress syndrome ROM rupture of membranes ROT right occiput transverse RPR rapid plasma reagin RR respiratory rate SAB spontaneous abortion SCC squamous cell carcinoma SERM selective estrogen receptor modulators SGA small for gestational age SHBG sex hormone binding globulin SIDS sudden infant death syndrome SLE systemic lupus erythematosus SNRIs serotonin-norepinephrine reuptake inhibitor SPT septic pelvic thrombophlebitis SROM spontaneous rupture of membranes SSRIs selective serotonin reuptake inhibitors STD sexually transmitted disease STI sexually transmitted infection SUI stress urinary incontinence SVT superficial vein thrombophlebitis SVT supraventricular tachycardia TAB therapeutic abortion TAC transabdominal cerclage TAHBSO total abdominal hysterectomy and bilateral salpingo-oophorectomy TBG thyroid binding globulin TENS transcutaneous electrical nerve stimulation TFTs thyroid function tests TIBC total iron-binding capacity TLC total lung capacity TNM tumor/node/metastasis TOA tubo-ovarian abscess TOLAC trial of labor after cesarean TOV transposition of the vessels tPA tissue plasminogen activator TPAL term, preterm, aborted, living TRH thyrotropin-releasing hormone TSE testicular sperm extraction TSH thyroid-stimulating hormone TSI thyroid-stimulating immunoglobulins TSS toxic shock syndrome TSST toxic shock syndrome toxin TTTS twin-to-twin transfusion syndrome UA urinalysis UAE uterine artery embolization UG urogenital UIQ upper inner quadrant UOQ upper outer quadrant UPI uteroplacental insufficiency US ultrasound UTI urinary tract infection V/Q ventilation/perfusion ratio VAIN vaginal intraepithelial neoplasia VBAC vaginal birth after cesarean VD volume of distribution VDRL Venereal Disease Research Laboratory VIN vulvar intraepithelial neoplasia VLDL very low density lipoprotein VS vital signs VSD ventricular septal defect VZIG varicella zoster immune globulin VZV varicella zoster virus WBC white blood cell XAFP expanded maternal serum alpha feto-protein (test) XR x-ray Chapter 1 Pregnancy and Prenatal Care PREGNANCY Pregnancy is the state of having products of conception implanted normally or abnormally in the uterus or occasionally elsewhere. Pregnancy is terminated by spontaneous or elective abortion or delivery. A myriad of physiologic changes occur in a pregnant woman, which affect every organ system. DIAGNOSIS In a patient who has regular menstrual cycles and is sexually active, a period delayed by more than a few days to a week is suggestive of pregnancy. Even at this early stage, patients may exhibit signs and symptoms of pregnancy. On physical examination, a variety of findings indicate pregnancy (Table 1-1). Many over-the-counter (OTC) urine pregnancy tests have a high sensitivity and will be positive around the time of the missed menstrual cycle. These urine tests and the hospital laboratory serum assays test for the beta subunit of human chorionic gonadotropin (β-hCG). This hormone produced by the placenta will rise to a peak of 100,000 mIU/mL by 10 weeks of gestation, decrease throughout the second trimester, and then level off at approximately 20,000 to 30,000 mIU/mL in the third trimester. A viable pregnancy can be confirmed by ultrasound, which may show the gestational sac as early as 5 weeks on a transvaginal ultrasound, or at a β-hCG of 1,500 to 2,000 mIU/mL, and the fetal heart as soon as 6 weeks, or a β-hCG of 5,000 to 6,000 mIU/mL. TERMS AND DEFINITIONS From the time of fertilization until the pregnancy is 8 weeks along (10 weeks gestational age [GA]), the conceptus is called an embryo. After 8 weeks until the time of birth, it is designated a fetus. The term infant is used for the period between delivery and 1 year of age. Pregnancy is divided into trimesters. The first trimester lasts until 12 weeks but is also defined as up to 14 weeks GA, the second trimester from 12 to 14 until 24 to 28 weeks GA, and the third trimester from 24 to 28 weeks until delivery. An infant delivered prior to 24 weeks is considered to be previable, from 24 to 37 weeks is considered preterm, and from 37 to 42 weeks is considered term. A pregnancy carried beyond 42 weeks is considered postterm. Gravidity (G) refers to the number of times a woman has been pregnant, and parity (P) refers to the number of pregnancies that led to a birth at or beyond 20 weeks GA or of an infant weighing more than 500 g. For example, a woman who has given birth to one set of twins would be a G1 P1, as a multiple gestation is considered as just one pregnancy. A more specific designation of pregnancy outcomes divides parity into term and preterm deliveries and also adds the number of abortuses and number of living children. This is known as the TPAL designation. Abortuses include all pregnancy losses prior to 20 weeks, both therapeutic and spontaneous, as well as ectopic pregnancies. For example, a woman who has given birth to one set of preterm twins, one term infant, and with two miscarriages would be a G4 P1-1-2-3. P.4 TABLE 1-1 Signs and Symptoms of Pregnancy Signs Bluish discoloration of vagina and cervix (Chadwick sign)  Softening and cyanosis of the cervix at or after 4 weeks (Goodell sign) Softening of the uterus after 6 weeks (Ladin sign) Breast swelling and tenderness Development of the linea nigra from umbilicus to pubis Telangiectasias Palmar erythema Symptoms Amenorrhea Nausea and vomiting Breast pain Quickening—fetal movement The prefixes nulli-, primi-, and multi- are used with respect to gravidity and parity to refer to having 0, 1, or more than 1, respectively. For example, a woman who has been pregnant twice, one ectopic pregnancy and one full term birth, would be multigravidous and primiparous. Unfortunately, this terminology often gets misused with individuals referring to women with a first pregnancy as primiparous, rather than nulliparous. Obstetricians also utilize the term “grand multip,” which refers to a woman whose parity is greater than or equal to 5. DATING OF PREGNANCY The GA of a fetus is the age in weeks and days measured from the last menstrual period (LMP). Developmental age (DA) or conceptional age or embryonic age is the number of weeks and days since fertilization. Because fertilization usually occurs about 14 days after the first day of the prior menstrual period, the GA is usually 2 weeks more than the DA. Classically, Nägele's rule for calculating the estimated date of confinement (EDC), or estimated date of delivery (EDD), is to subtract 3 months from the LMP and add 7 days. Thus, a pregnancy with an LMP of 8/05/08 would have an EDC of 5/12/09. Exact dating uses an EDC calculated as 280 days after a certain LMP. If the date of ovulation is known, as in assisted reproductive technology (ART), the EDC can be calculated by adding 266 days. Pregnancy dating can be confirmed and should be consistent with the examination of the uterine size at the first prenatal appointment. With an uncertain LMP, ultrasound is often used to determine the EDC. Ultrasound has a level of uncertainty that increases during the pregnancy but it is rarely off by more than 7% to 8% at any GA. A safe rule of thumb is that the ultrasound should not differ from LMP dating by more than 1 week in the first trimester, 2 weeks in the second trimester, and 3 weeks in the third trimester. The dating done with crown-rump length in the first half of the first trimester is probably even more accurate, to within 3 to 5 days. Other measures used to estimate gestational age include pregnancy landmarks such as auscultation of the fetal heart (FH) at 20 weeks by nonelectronic fetoscopy or at 10 weeks by Doppler ultrasound, as well as maternal awareness of fetal movement or “quickening,” which occurs between 16 and 20 weeks. Because ultrasound dating of pregnancy only decreases in accuracy as the pregnancy progresses, determining and confirming pregnancy dating at the first interaction between a pregnant women and the healthcare system is imperative. A woman who presents to the emergency department may not return for prenatal care, so dating confirmation should occur at that visit. Pregnancy dating is particularly important because a number of decisions regarding care are based on accurate dating. One such decision is whether to resuscitate a newborn at the threshold of viability, which may be at 23 or 24 weeks of gestation depending on the institution. Another is the induction of labor at 41 weeks of gestation. Since 5% to 15% of women may be oligo-ovulatory, they ovulate beyond the usual 14th day of the cycle. Thus, their LMP dating may overdiagnose a prolonged (≥41 weeks' gestation) or postterm pregnancy (≥42 weeks' gestation). Thus, early verification or correction of dating can correct such misdating. PHYSIOLOGY OF PREGNANCY Cardiovascular During pregnancy, cardiac output increases by 30% to 50%. Most increases occur during the first trimester, P.5 with the maximum being reached between 20 and 24 weeks' gestation and maintained until delivery. The increase in cardiac output is first due to an increase in stroke volume then is maintained by an increase in heart rate as stroke volume decreases to near prepregnancy levels by the end of the third trimester. Systemic vascular resistance decreases during pregnancy, resulting in a fall in arterial blood pressure. This decrease is most likely due to the elevated progesterone leading to smooth muscle relaxation. There is a decrease in systolic blood pressure of 5 to 10 mm Hg and in diastolic blood pressure of 10 to 15 mm Hg that nadirs at week 24. Between 24 weeks' gestation and term, blood pressure slowly returns to prepregnancy levels but should never exceed them. Pulmonary There is an increase of 30% to 40% in tidal volume (VT) during pregnancy (Fig. 1-1) despite the fact that the total lung capacity is decreased by 5% due to the elevation of the diaphragm. This increase in V T decreases the expiratory reserve volume by about 20%. The increase in VT with a constant respiratory rate leads to an increase in minute ventilation of 30% to 40%, which in turn leads to an increase in alveolar (PAo2 ) and arterial (Pao 2 ) Po2 levels and a decrease in PAco2 and Paco 2 levels. Paco 2 decreases to approximately 30 mm Hg by 20 weeks' gestation from 40 mm Hg prepregnancy. This change leads to an increased CO2 gradient between mother and fetus and is likely caused by elevated progesterone levels that either increase the respiratory system's responsiveness to CO2 or act as a primary stimulant. This gradient facilitates oxygen delivery to the fetus and carbon dioxide removal from the fetus. Dyspnea of pregnancy occurs in 60% to 70% of patients. This is possibly secondary to decreased Paco 2 levels, increased V T , or decreased total lung capacity (TLC).  Figure 1-1 Lung volumes in nonpregnant and pregnant women. Gastrointestinal Nausea and vomiting occur in more than 70% of pregnancies. This has been termed “morning sickness” even though it can occur anytime throughout the day. These symptoms have been attributed to the elevation in estrogen, progesterone, and hCG. It may also be due to hypoglycemia and can be treated with frequent snacking. The nausea and vomiting typically resolve by 14 to 16 weeks' gestation. Hyperemesis gravidarum refers to a severe form of morning sickness in which women lose greater than 5% of their prepregnancy weight and go into ketosis. During pregnancy, the stomach has prolonged gastric emptying times, and the gastroesophageal sphincter has decreased tone. Together, these changes lead to reflux and possibly combine with decreased esophageal tone to cause ptyalism, or spitting, during pregnancy. The large bowel also has decreased motility, which leads to increased water absorption and constipation. Renal The kidneys increase in size and the ureters dilate during pregnancy, which may lead to increased rates of pyelonephritis. The glomerular filtration rate (GFR) increases by 50% early in pregnancy and is maintained until delivery. As a result of increased P.6 GFR, blood urea nitrogen and creatinine decrease by about 25%. An increase in the renin-angiotensin system leads to increased levels of aldosterone, which results in increased sodium resorption. However, plasma levels of sodium do not increase because of the simultaneous increase in GFR. Hematology Although the plasma volume increases by 50% in pregnancy, the red blood cell volume increases by only 20% to 30%, which leads to a decrease in the hematocrit, or dilutional anemia. The white blood cell (WBC) count increases during pregnancy to a mean of 10.5 million/mL with a range of 6 to 16 million. During labor, stress may cause the WBC count to rise to over 20 million/mL. There is a slight decrease in the concentration of platelets, probably secondary to increased plasma volume and an increase in peripheral destruction. Although 7% to 8% of patients' platelets may be between 100 and 150 million/mL, a drop in the platelet count below 100 million/mL or over a short time period is not normal and should be investigated promptly. Pregnancy is considered to be a hypercoagulable state, and the number of thromboembolic events increases. There are elevations in the levels of fibrinogen and factors VII-X. However, the actual clotting and bleeding times do not change. The increased rate of thromboembolic events in pregnancy may also be secondary to the other elements of Virchow triad, an increase in venous stasis and vessel endothelial damage. Endocrine Pregnancy is a hyperestrogenic state. The increased estrogen is produced primarily by the placenta, with the ovaries contributing to a lesser degree. Unlike estrogen production in the ovaries, where estrogen precursors are produced in ovarian theca cells and transferred to the ovarian granulosa cells, estrogen in the placenta is derived from circulating plasma-borne precursors produced by the maternal adrenal glands. Fetal well-being has been correlated with maternal serum estrogen levels with low estrogen levels being associated with conditions such as fetal death and anencephaly. The hormone hCG is composed of two dissimilar alpha and beta subunits. The alpha subunit of hCG is identical to the alpha subunits of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and thyroid-stimulating hormone (TSH), whereas the beta subunits differ. Levels of hCG double approximately every 48 hours during early pregnancy, reaching a peak at approximately 10 to 12 weeks, and thereafter declining to reach a steady state after week 15. The placenta produces hCG, which acts to maintain the corpus luteum in early pregnancy. The corpus luteum produces progesterone, which maintains the endometrium. Eventually the placenta takes over progesterone production and the corpus luteum degrades into the corpus albicans. Progesterone levels increase over the course of pregnancy. Progesterone causes relaxation of smooth muscle, which has multiple effects on the gastrointestinal, cardiovascular, and genitourinary systems. Human placental lactogen (hPL) is produced in the placenta and is important for ensuring a constant nutrient supply to the fetus. hPL, also known as human chorionic somatomammotropin (hCS), causes lipolysis with a concomitant increase in circulating free fatty acids. hPL also acts as an insulin antagonist, along with various other placental hormones, thereby having a diabetogenic effect. This leads to increased levels of insulin and protein synthesis. Levels of prolactin are markedly increased during pregnancy. These levels decrease after delivery but later increase in response to suckling. There are two major changes in thyroid hormones during pregnancy. First, estrogen stimulates thyroid binding globulin (TBG) leading to an elevation in total T3 and T4 but free T3 and T4 remain relatively constant. Second, hCG has a weak stimulating effect on the thyroid, likely as its alpha subgroup is similar to TSH. This leads to a slight increase in T3 and T4 and a slight decrease in TSH early in pregnancy. Overall, however, pregnancy is considered a euthyroid state. Musculoskeletal and Dermatologic The obvious change in the center of gravity during pregnancy can lead to a shift in posture and lower back strain. Numerous changes in the skin occur during pregnancy, including spider angiomata and palmar erythema secondary to increased estrogen levels and hyperpigmentation of the nipples, umbilicus, abdominal midline (the linea nigra), perineum, and face (melasma or chloasma) secondary to increased levels of melanocyte-stimulating hormone and the steroid hormones. P.7 Nutrition Nutritional requirements increase during pregnancy and breastfeeding. The average woman requires 2,000 to 2,500 kcal/day. The caloric requirement is increased by 300 kcal/day during pregnancy and by 500 kcal/day when breastfeeding. Most patients should gain between 20 and 30 pounds during pregnancy. Overweight women are advised to gain less, between 15 and 25 pounds; underweight women are advised to gain more, 28 to 40 pounds. In addition to the increased caloric requirements, there are increased nutritional requirements for protein, iron, folate, calcium, and other vitamins and minerals. The protein requirement increases from 60 g/day to 70 or 75 g/day. Recommended calcium intake is 1.5 g/day. Many patients develop iron deficiency anemia because of the increased demand on hematopoiesis both by the mother and the fetus. Folate requirements increase from 0.4 to 0.8 mg/day and are important in preventing neural tube defects. TABLE 1-2 Recommended Daily Dietary Allowances for Nonpregnant, Pregnant, and Lactating Women Nonpregnant Women by Age Pregnant Lactating  11 to 14 15 to 18 19 to 22 23 to 50 51+ Women Women Energy (kcal) 2,400 2,100 2,100 2,000 1,800 +300 +500 Protein (g) 44 48 46 46 46 +30 +20 Fat-soluble vitamins 800 800 800 800 800 1,000 1,200 Vitamin A activity (RE) (IU) 4,000 4,000 4,000 4,000 4,000 5,000 6,000 Vitamin D (IU) 400 400 400 — — 400 400 Vitamin E activity (IU) 12 12 12 12 12 15 15 Water- soluble vitamins Ascorbic acid (mg) 45 45 45 45 45 60 80 Folacin (µg) 400 400 400 400 400 800 600 Niacin (mg) 16 14 14 13 12 +2 +4 Riboflavin (mg) 1.3 1.4 1.4 1.2 1.1 +0.3 +0.5 Thiamin (mg) 1.2 1.1 1.1 1 1 +0.3 +0.3 Vitamin B 6 (mg) 1.6 2 2 2 2 2.5 2.5 Vitamin B12 (µg) 3 3 3 3 3 4 4  Minerals Calcium (mg) 1,200 1,200 800 800 800 1,200 1,200 Iodine (µg) 115 115 100 100 80 125 150 Iron (mg) 18 18 18 18 10 +18 18 Magnesium (mg) 300 300 300 300 300 450 450 Phosphorus (mg) 1,200 1,200 800 800 800 1,200 1,200 Zinc (mg) 15 15 15 15 15 20 25 From Gabbe SG, Niebyl JR, Simpsen JL. Obstetrics: Normal and Problem Pregnancies, 4th ed. New York: Churchill Livingstone, 2002:196. IU, International Unit. All patients are advised to take prenatal vitamins during pregnancy. These are designed to compensate for the increased nutritional demands of pregnancy. Furthermore, any patient whose hematocrit falls during pregnancy is advised to increase iron intake with oral supplementation (Table 1-2). P.8 PRENATAL CARE Prenatal visits are designed to screen for various complications of pregnancy and to educate the patient. They include a series of outpatient office visits that involve routine physical examinations and various screening tests that occur at different points in the prenatal care. Important issues of prenatal care include initial patient evaluation, routine patient evaluation, nutrition, disease states during the pregnancy, and preparing for the delivery. INITIAL VISIT This is often the longest of the prenatal visits because it involves obtaining a complete history and performing a physical as well as a battery of initial laboratory tests. It should occur early in the first trimester, between 6 and 10 weeks, although occasionally patients will not present for their initial prenatal visit until later in their pregnancy. History The patient's history includes the present pregnancy, the last menstrual period, and symptoms during the pregnancy. After this, an obstetric history of prior pregnancies including date, outcome (e.g., SAB [spontaneous abortion], TAB [therapeutic abortion], ectopic pregnancy, term delivery), mode of delivery, length of time in labor and second stage, birth weight, and any complications. Finally, a complete medical, surgical, family, and social history should be obtained. Physical Examination A complete physical examination is performed, paying particular attention to the patient's prior medical and surgical history. The pelvic examination includes a Pap smear, unless one has been done in the past 6 months, and cultures for gonorrhea and chlamydia. On bimanual examination, the size of the uterus should be consistent with the gestational age from the LMP. If a woman is unsure of her LMP or size and dates are not consistent, one should obtain an ultrasound for dating. Accurate dating is crucial for all subsequent obstetrical evaluations and interventions. Diagnostic Evaluation The panel of tests in the first trimester includes a complete blood count, primarily for hematocrit, blood type, antibody screen, rapid plasma reagin (RPR) or VDRL screening for syphilis, rubella antibody screen, hepatitis B surface antigen, urinalysis, and urine culture. If a patient has no history of chickenpox, a titer for varicella zoster virus (VZV) antibodies is sent. A purified protein derivative (PPD) is usually placed during the first or second trimester. A urine pregnancy test should be sent if the patient is not entirely certain she is pregnant. If there has been any bleeding or cramping, a β-hCG level should be obtained. While there is some debate over the use of routine toxoplasma titers, they are often ordered as well. All patients are counseled about human immunodeficiency virus (HIV) and testing should be offered routinely (Table 1-3). In addition, first trimester screening tests for aneuploidy with nuchal translucency (NT) by ultrasound and serum markers are increasingly being obtained in most women via referral to a prenatal diagnosis unit. In addition to this battery of tests, there are a variety of other screens offered to high-risk patients (Table 1-4). ROUTINE PRENATAL VISITS Blood pressure, weight, urine dipstick, measurement of the uterus, and auscultation of the fetal heart are performed and assessed on each follow-up prenatal care visit. Maternal blood pressure decreases during the first and second trimester and slowly returns to baseline during the third trimester; elevation may be a sign of preeclampsia. Maternal weight is followed serially throughout the pregnancy as a proxy for adequate nutrition. Also, large weight gains toward the end of pregnancy can be a sign of fluid retention and preeclampsia. Measurement of the uterine fundal height in centimeters corresponds roughly to the weeks of gestation. If the fundal height is progressively decreasing or is 3 cm less than gestational age, an ultrasound is done to more accurately assess fetal growth. After 10 to 14 weeks, Doppler ultrasound is used to auscultate the fetal heart rate. Urine is routinely dipped for protein, glucose, blood, and leukocyte esterase. Protein may be indicative of preeclampsia, glucose of diabetes, and leukocyte esterase of urinary tract infection (UTI). Pregnant women are at an increased risk for complicated UTIs such as pyelonephritis given increased urinary stasis P.9 from mechanical compression of the ureters and progesterone-mediated smooth muscle relaxation. TABLE 1-3 Routine Tests in Prenatal Care Third Initial Visit and First Trimester Second Trimester Trimester MSAFP/triple or quad Hematocrit screen Hematocrit Blood type and screen Obstetric ultrasound RPR/VDRL RPR/VDRL Amniocentesis for women GLT interested in prenatal diagnosis Group B strep Rubella antibody screen culture  Hepatitis B surface antigen Gonorrhea culture Chlamydia culture PPD Pap smear Urinalysis and culture VZV titer in patients with no history of exposure HIV offered Early screening for aneuploidy (nuchal translucency plus serum markers) TABLE 1-4 Initial Screens in Specific High-Risk Groups High-Risk Group Specific Test African American, Southeast Asian, MCV Sickle-cell prep for African 6). After 42 weeks of gestation, the patient is induced regardless of cervical examination. Increasingly, patients are induced between 41 and 42 weeks, as a result of improved dating by ultrasound, patient demand, as well as the risk-averse environment of obstetrics. Several randomized trials have demonstrated that induction of labor at 41 weeks of gestation as compared to expectant management leads to lower rates of cesarean delivery as well as lower rates of meconium aspiration syndrome in the neonate. However, in the face of this evidence, 42 weeks of gestation is still utilized by ACOG as the definition of postterm. MULTIPLE GESTATIONS If a fertilized ovum divides into two separate ova, monozygotic, or “identical,” twins result. If ovulation produces two ova and both are fertilized, dizygotic twins result. Without assisted fertility, the rate of twinning is approximately 1:80 pregnancies, with 30% of those monozygotic. The rate of naturally occurring triplets is approximately 1:7,000 to 8,000 pregnancies. However, with ovulation-enhancing drugs and in vitro fertilization (IVF), the incidence of multiple gestations is increasing. COMPLICATIONS OF MULTIPLE GESTATION Multiple gestations result in an increase in a variety of obstetric complications including preterm labor, placenta previa, cord prolapse, postpartum hemorrhage, cervical incompetence, gestational diabetes, and preeclampsia. The fetuses are at increased risk for preterm delivery, congenital abnormalities, SGA, and malpresentation. The average gestational age of delivery for twins is between 36 and 37 weeks; for triplets it is 33 to 34 weeks. Monochorionic (one placenta), diamnionic (two amniotic sacs) twins, also referred to as MoDi twins, often have placental vascular communications and can develop twin-to- twin transfusion syndrome (TTTS). Monochorionic, monoamnionic (Mo-Mo) twins have an extremely high mortality rate (40% to 60%) secondary to cord accidents from entanglement. Pathogenesis Monozygotic twinning results from division of the fertilized ovum or cells in the embryonic disk. If separation occurs before the differentiation of the trophoblast, two chorions and two amnions (Di-Di) result (Fig. 7-6). After trophoblast differentiation and before amnion formation (days 3 to 8), separation leads to a single placenta, one chorion, and two amnions (Mo-Di). Division after amnion formation leads to a single placenta, one chorion, and one amnion (Mo-Mo) (days 8 to 13) and rarely, conjoined or “Siamese” twins (days 13 to 15). Division of cells beyond day 15 or 16 will result in a singleton fetus. Monozygotic twinning does not follow any inheritable pattern and, historically, the only risk factor ever identified is a slight increase with advancing maternal age. In the 1990s it was determined that assisted reproductive techniques, while increasing the risk of dizygotic twins, also increases the risk of monozygotic twins to as high as 5%. Dizygotic twins primarily result from fertilization of two ova by two sperm. There are varying risk factors associated with dizygotic twinning. Dizygotic twins tend to run in families and are more common in people of African descent. Globally, the rate of dizygotic twins ranges from 1:1,000 in Japan to 1:20 in several Nigerian tribes. The rate of all multiple gestations has increased sharply since the onset of medical treatment of infertility. Clomiphene citrate, a fertility-enhancing drug, increases the rate of dizygotic twinning up to 8%. However, the utilization of multiple embryos in the setting of IVF in order to improve the pregnancy rates leads to rates of twinning and higher order multiple gestations in 30% to 50% of these pregnancies. Diagnosis Multiple gestations are usually diagnosed by ultrasound. Multiple gestations are indicated by rapid uterine growth, excessive maternal weight gain, or P.89 palpation of three or more fetal large parts (cranium and breech) on Leopold's. The level of β-hCG, human placental lactogen (HPL), and maternal serum α-fetoprotein (MSAFP) are all elevated for gestational age. Rarely, diagnosis will be made after delivery of the first fetus with palpation of the aftercoming fetus(es). Differentiation between Di-Di and Mo-Di twins is easier the earlier the ultrasound is performed. For example, quite early in pregnancy, one can see a single chorion and two amniotic sacks (Fig. 7-7) indicative of Mo-Di twins. Later in pregnancy, sonologists rely on the thickness of the membrane and the “twin peak” sign (Fig 7-8), which is formed by the two placentae fusing together in the setting of Di-Di twins. Mo-Mo twins are usually easiest as they should have no intertwin membrane. Figure 7-6 The relationship between the timing of cleavage and the resulting amnionicity/chorionicity in monozygotic twinning. (From LifeART image copyright © 2006 Lippincott Williams & Wilkins. All rights reserved.) Treatment Because of the increased risk of complications, multiple-gestation pregnancies are managed as high-risk pregnancies, usually in conjunction with a perinatologist. Aside from the antenatal management of the complications, the principal issue in twin gestations is mode of delivery. With higher order multiple gestations, triplets and above, selective reduction down to twins or even a singleton, is commonly recommended. While there is a chance of losing the entire pregnancy in the setting of selective reduction, if successful, the chances of delivering a severely premature infant is also dramatically reduced. However, the question of the risks and benefits of selective reduction from twins to a singleton gestation is unanswered at this time. Figure 7-7 Monochorionic-diamniotic (Mo-Di) twins: Note the single chorion, but two developing amniotic sacs. P.90 Figure 7-8 The fused chorionic and amniotic membranes lead to the “twin peak” sign in the middle of image in Di-Di twins. TWIN-TO-TWIN TRANSFUSION SYNDROME (TTTS) Polyhydramnios-oligohydramnios (poly-oli) sequence or TTTS has been described for several centuries and results in a small, anemic twin and a large, plethoric, polycythemic, and occasionally hydropic twin. The etiology of TTTS appears to be secondary to unequal flow within vascular communications between the twins in their shared placenta leading to one twin becoming a donor and the other a recipient of this unequal blood flow. This can result in one fetus with hypervolemia, cardiomegaly, glomerulotubal hypertrophy, edema, and ascites and the other with hypovolemia, growth restriction, and oligohydramnios. Because of the risk of this syndrome in Mo-Di twins, serial ultrasounds examining the amniotic fluid and fetal growth should be obtained every 2 weeks after diagnosis. TTTS has historically been managed with serial amnioreduction, which can reduce preterm contractions secondary to uterine distension and maternal symptoms, but only occasionally actually cures the fetal syndrome. More recently, as these vascular connections have been identified as the etiology of the syndrome, coagulating these vessels has been proposed as the treatment of choice in more severe cases. This is accomplished by fetal surgeons using a fetoscopically placed laser to coagulate the vessels. While this procedure carries risks both to the mother and of losing the pregnancy entirely or eventual preterm delivery, TTTS itself almost inevitably will lead to extremely poor pregnancy outcomes, so it appears to be, on balance, beneficial to these patients. However, because of the potential risks, pregnancy termination should always be offered as an option as well in the setting of TTTS. MO-MO TWINS Because of the risk of cord entanglement and IUFD, Mo-Mo twins are often managed with frequent antenatal testing and early delivery. Unfortunately, frequent antenatal testing has not in and of itself appeared to make a difference in the rate of IUFD in these cases. Because of this, some patients are offered admission to the hospital and continuous electronic fetal monitoring from weeks 28 to 34, at which time delivery is performed via cesarean section. Mo-Mo and conjoined twins are almost always delivered via cesarean section. DELIVERY OF TWINS There are four possibilities for twin presentation: both vertex (40%), both breech, vertex then breech (40%), and breech then vertex. When deciding mode of delivery, all breech-presenting twins (20%) are considered together. Vertex/vertex twins should undergo a trial of labor with cesarean section reserved for the usual indications. Vertex/nonvertex twins can also undergo a trial of labor if the twins are concordant or the presenting twin is larger. Generally, the twins should be between 1,500 g and 3,500 g, though there is scant data that breech extraction between 500 g and 1,500 g leads to any worse outcomes. Breech extraction for delivery of the second twin has advantages over a vertex second twin because the twin B's lower extremity can be grasped and delivery expedited quickly. In the setting of a vertex second twin, occasionally, placental abruption occurs necessitating a rapid delivery. But if the cervix is no longer fully dilated or the fetal vertex is above 0 station, a cesarean delivery may be P.91 necessary. External cephalic version and internal podalic version have also been used for delivery of the second twin, but in small studies lower Apgar scores have been found as compared to breech extraction. Further, the chances of failure of such maneuvers is higher. Nonvertex presenting twins are usually delivered via cesarean. DELIVERY OF TRIPLETS Most triplet gestations are delivered via cesarean section. Rarely, triplets will be concordant, with vertex presenting, all greater than 1,500 g to 2,000 g and a vaginal delivery can be attempted. Multiple gestations beyond triplets are all delivered via cesarean. KEY POINTS Fetuses whose EFW is less than the 10th percentile are considered small for gestational age (SGA), though the rate of poor neonatal outcomes rises significantly below the 5th and 3rd percentiles. Common causes of decreased growth potential include congenital abnormalities, drugs, infections, radiation, and small maternal stature. IUGR infants are commonly born to women with systemic diseases leading to poor placental blood flow. An LGA fetus has an EFW greater than the 90th percentile at any particular gestational age. Both 4,000 g and 4,500 g have been used as the threshold for defining fetal macrosomia. LGA and macrosomic fetuses are at greater risk for birth trauma, hypoglycemia, jaundice, lower Apgar scores, and childhood tumors. Increased size in the fetus is seen with maternal diabetes, maternal obesity, increased maternal height, postterm pregnancies, multiparity, advanced maternal age, and male sex. Oligohydramnios is defined by an AFI of less than 5 and can be caused by decreased placental perfusion, decreased fluid production by the fetus, and rupture of membranes. Pregnancies at term complicated by oligohydramnios should be delivered. Polyhydramnios is diagnosed by an AFI greater than 20 on ultrasound and is associated with diabetes, multiple gestations, hydrops, and congenital abnormalities. Obstetric management of polyhydramnios should include careful verification of presentation and close observation for cord prolapse. Rh sensitized women with Rh-positive fetuses have antibodies that cross the placenta, leading to hemolysis and anemia in the fetuses. If the anemia is severe enough, hydrops develops with edema, ascites, and heart failure. Rh-negative patients who are not sensitized should be treated with antepartum RhoGAM to prevent sensitization. Postpartum, they should receive another dose of RhoGAM if the fetus is Rh positive. Rh-negative patients undergoing miscarriage, abruption, amniocentesis, ectopic pregnancy, and vaginal bleeding should also be given RhoGAM. Rh-negative patients who are sensitized are followed closely with serial ultrasounds and amniocentesis. The amniocentesis is done to measure the amount of bilirubin in the fluid, which is indicative of the amount of hemolysis. While IUFD is more common with disorders of the placenta the actual cause of most IUFDs is usually unknown and is often attributed to cord accidents. Retained IUFD can lead to DIC; thus, delivery soon after diagnosis is indicated. Postterm pregnancy is defined as greater than 42 weeks' gestational age. Postterm pregnancies are at increased risk for fetal demise, macrosomia, meconium aspiration, and oligohydramnios. Increased fetal surveillance and labor induction are the most common management options for postterm pregnancies. Monozygotic twins carry identical genetic material, whereas dizygotic twins are from separate ova and sperm. Multiple gestations are at increased risk for preterm labor and delivery, placenta previa, postpartum hemorrhage, preeclampsia, cord prolapse, malpresentation, and congenital abnormalities. There is a genetic predisposition for dizygotic twinning, whereas the rate of monozygotic twinning is the same throughout all races and families. Monozygotic twins are at risk for TTTS, and should have frequent ultrasound examinations to diagnose this early. Vaginal delivery of vertex/vertex presenting twins is preferred and is possible with vertex/nonvertex twins under the right circumstances. Nonvertex presenting twins are delivered by cesarean section. Chapter 8 Hypertension and Pregnancy Blood pressure in pregnancy is usually decreased. As a result of decreased vascular resistance, the blood pressure decreases in the latter half of the first trimester reaching its nadir in the mid-second trimester. During the third trimester, blood pressure will usually increase, but should not be higher than prepregnancy. Hypertension may be present before pregnancy—as with chronic hypertension, or may be induced by pregnancy—as with gestational hypertension (GH), preeclampsia, and eclampsia (Table 8-1). Liver injury is seen in a small percentage of patients with preeclampsia and is associated with two diseases in pregnancy with high morbidity and mortality: HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) and acute fatty liver of pregnancy. Complications from these disorders are consistently among the leading causes of maternal death in developed countries. Because treatment is delivery, these disorders are also leading causes of premature delivery. PREECLAMPSIA PATHOGENESIS Preeclampsia is the presence of nondependent edema, hypertension, and proteinuria in the pregnant woman. While this triad is typically how women present, non-dependent edema is no longer a component of the diagnosis. The classic presentation is of a nulliparous woman in her third trimester. Although no definitive cause for preeclampsia has been determined, it is well accepted that the underlying pathophysiology involves a generalized arteriolar constriction (vasospasm) and intravascular depletion secondary to a generalized transudative edema that can produce symptoms related to ischemia, necrosis, and hemorrhage of organs. Thus, one of the fundamental aspects of the disease is vascular damage and an imbalance in the relative concentrations of prostacyclin and thromboxane. It is theorized that this is primarily related to circulating antibodies or antigen-antibody complexes (not unlike systemic lupus erythematosus) that damage the lining of vessel walls leading to exposure of the underlying collagen structure. The hyperdynamic state of pregnancy has also been proposed to cause this underlying vascular injury rather than an immunogenic phenomenon. As outlined in Table 8-2, major fetal complications of preeclampsia are due to prematurity. Also, the generalized vasoconstriction of preeclampsia can result in decreased blood flow to the placenta. This may manifest as acute uteroplacental insufficiency, resulting in abruption or fetal distress. The uteroplacental insufficiency may also be chronic in nature and result in an intrauterine growth restricted (IUGR) fetus. Maternal complications associated with preeclampsia (Table 8-3) are related to the generalized arteriolar vasoconstriction that affects the brain (seizure and stroke), kidneys (oliguria and renal failure), lungs (pulmonary edema), liver (edema and subcapsular hematoma), and small blood vessels (thrombocytopenia and disseminated intravascular coagulation [DIC]). Severe preeclampsia is diagnosed with severely elevated blood pressures, defined as SBP >160 or DBP >110 or the presence of any of the above clinical findings. About 10% of patients with severe preeclampsia develop HELLP syndrome. HELLP syndrome is a subcategory of preeclampsia in which the patient presents with hemolysis, elevated liver enzymes, and low platelets. Hypertension and proteinuria may be P.93 minimal in these patients. HELLP syndrome is uncommon, but patients who experience it decline rapidly, resulting in poor maternal and fetal outcomes. Despite careful management, HELLP syndrome results in a high rate of stillbirth (10% to 15%) and neonatal death (20% to 25%). TABLE 8-1 Hypertensive States of Pregnancy Pregnancy-induced (or gestational) hypertension  Preeclampsia Severe preeclampsia Chronic hypertension Chronic hypertension w/superimposed preeclampsia HELLP syndrome AFLP EPIDEMIOLOGY Preeclampsia occurs in 5% to 6% of all live births and can develop any time after the 20th week, but is most commonly seen in the third trimester near term. When hypertension is seen early in the second trimester (14 to 20 weeks), a hydatidiform mole or previously undiagnosed chronic hypertension should be considered. Unlike other preeclamptic patients, the patient with HELLP is more likely to be less than 36 weeks' gestation at the time of presentation. Although 80% of patients develop HELLP after being diagnosed with preeclampsia (30% with mild preeclampsia; 50% with severe preeclampsia), 20% of patients with HELLP have no previous history of hypertension before their diagnosis, and will present merely with the symptom of right upper-quadrant pain. TABLE 8-2 Fetal Complications of Preeclampsia Complications related to prematurity (if early delivery is necessary) Acute uteroplacental insufficiency Placental infarct and/or abruption Intrapartum fetal distress Stillbirth (in severe cases) Chronic uteroplacental insufficiency Asymmetric and symmetric SGA fetuses IUGR  Oligohydramnios TABLE 8-3 Maternal Complications of Preeclampsia Medical manifestations Seizure Cerebral hemorrhage DIC and thrombocytopenia Renal failure Hepatic rupture or failure Pulmonary edema Obstetric complications Uteroplacental insufficiency Placental abruption Increased premature deliveries Increased cesarean section deliveries RISK FACTORS Risk factors for preeclampsia fall essentially into two categories: those related to the manifestations of the disease (like chronic hypertension or renal disease), and those related to the immunogenic nature of preeclampsia (Table 8-4). These latter risk factors are quite interesting. For example, it has been shown that in addition to a family history in the parturient, if the mother of the father of her baby (mother-in-law) had preeclampsia, the patient is at greater risk of developing preeclampsia. Further, it has been demonstrated that parental ethnic discordance slightly increases the risk of developing preeclampsia. While multiparous women who have not had preeclampsia in the past have a decreased risk, if a woman conceives with a new father of her baby, her risk increases back to that of a nullipara. A tolerance effect is seen in women who cohabitate with the father of the baby longer than 1 year prior to conceiving in comparison to women who conceive sooner. These risk factors P.94 support the theory that preeclampsia has an alloimmunogenic pathophysiology. TABLE 8-4 Risk Factors for Preeclampsia Primarily disease related Chronic hypertension Chronic renal disease Collagen vascular disease (e.g., SLE) Pregestational diabetes African American Maternal age (35) Primarily immunogenic related Nulliparity Previous preeclampsia Multiple gestation Abnormal placentation New paternity Family history Female relatives of parturient Mother-in-law Cohabitation less than 1 year CLINICAL MANIFESTATIONS AND DIAGNOSES Gestational Hypertension Blood pressures elevated above 140/90 are necessary to diagnose GH (formerly known as pregnancy-induced hypertension [PIH]). Blood pressures should be elevated on at least two occasions 4 to 6 hours apart and taken while the patient is seated. In the past an increase of 30 mm Hg above prepregnancy systolic BP or 15 mm Hg above prepregnancy diastolic BP had been utilized as well to identify GH. Currently, these changes are not recognized as diagnostic, but should still be noted clinically. If the patient's 24-hour urinary protein total is 300 mg/24 hr, well above 90% of the P.95 time. While an abnormal urine dip for protein is concerning, a negative urine dip should be less reassuring in the setting of hypertension. In one study, more than two-thirds of patients with elevated blood pressures and negative or trace on urine dip had greater than 300 mg/24 hr of urine protein and all patients with 3+ and 4+ protein had significant proteinuria. A better predictor of significant proteinuria is the urine protein to creatinine ratio. Because creatinine excretion is relatively constant, this ratio gives a rough estimate of the amount of protein that will be excreted over a 24-hour period. Ratios from 0.2 to 0.3 have been used as thresholds. TABLE 8-5 Criteria for Diagnosis of Gestational Hypertension, Preeclampsia, and Eclampsia Gestational hypertension Blood Pressure: SBP >140 OR DBP >90 Mild preeclampsia Blood Pressure: SBP >140 OR DBP >90 Proteinuria: >300 mg/24 hr or >1 to 2 plus on dipstick Severe preeclampsia (by systems) Neuro: Severe headache (not relieved by acetaminophen) Visual changes; scotomata  Cardiovascular: SBP >160 OR DBP >110 Pulmonary: Pulmonary edema Renal: Acute renal failure with rising creatinine Oliguria 2 times normal), oliguria (300 mg/day). It has an incidence of 5% to 6% of all live births and occurs most commonly in nulliparous women in their third trimester. Preeclampsia is characterized by a generalized multiorgan vasospasm that can lead to seizure, stroke, renal failure, liver damage, DIC, or fetal demise. Risk factors include nulliparity, multiple gestation, and chronic hypertension. Preeclampsia is ultimately treated with delivery, but seizures can be prevented with magnesium sulfate and blood pressures controlled with antihyperten-sive medications. Eclampsia is the occurrence of grand mal seizures in the preeclamptic patient that cannot be attributed to other causes. Patients present with seizures occurring before labor (25%), during labor (50%), or after delivery (25%). Eclampsia is treated with seizure management and prophylaxis with magnesium sulfate, hypertension management with hydralazine, and vaginal delivery only after the patient has been stabilized. Chronic hypertension is defined as hypertension occurring before conception, before 20 weeks' gestation, or persisting more than 6 weeks' postpartum. Chronic hypertension leads to superimposed preeclampsia in one-third of patients. Chronic hypertension is generally treated with antihypertensives, commonly nifedipine or labetalol. A baseline ECG and 24-hour urine collection for protein and creatinine should be performed. Chapter 9 Diabetes During Pregnancy Diabetes during pregnancy encompasses a range of disease entities that include gestational diabetes and overt diabetes mellitus (Table 9-1). In the nonpregnant state, diabetics are subgrouped into two types based on the pathophysiology of their disease, whereas during pregnancy, diabetes is usually characterized as pregestational or gestational diabetes. Pregestational diabetics include all patients with type 1 and type 2 diabetes diagnosed prior to pregnancy. Gestational diabetics are those diagnosed with carbohydrate intolerance during pregnancy. Due to a lack of routine screening for diabetes in many nonpregnant women, this latter group may occasionally include women with undiagnosed pregestational diabetes mellitus. GESTATIONAL DIABETES MELLITUS True gestational diabetes mellitus (GDM) is an impairment in carbohydrate metabolism that first manifests during pregnancy. These patients may have borderline carbohydrate metabolism impairment at baseline or be entirely normal in the nonpregnant state. However, during pregnancy, human chorionic somatomammotropin (a.k.a. human placental lactogen) and other hormones produced by the placenta act as anti-insulin agents leading to increased insulin resistance and generalized carbohydrate intolerance. Because these hormones increase in volume with the size and function of the placenta, the carbohydrate metabolism abnormalities usually are not apparent until the late second trimester or early third trimester. Thus, women with gestational diabetes generally are not at increased risk for congenital anomalies like women with pregestational diabetes. They do, however, carry an increased risk of fetal macrosomia and birth injuries as well as neonatal hypoglycemia, hypocalcemia, hyperbilirubinemia, and polycythemia like those with pregestational diabetes. Further, these women have a four- to tenfold increased risk of developing type 2 diabetes during their lifetime. EPIDEMIOLOGY The incidence of GDM ranges from 1% to 12% of pregnant women depending on the population. In the United States, it often has been reported to range between 5% and 8%. Gestational diabetes is seen at higher rates in women of Hispanic/Latina, Asian/Pacific Islander, and Native American descent, increasing maternal age, obesity, family history of diabetes, history of a previous infant weighing more than 4,000 g, and previous stillborn infant. Initial studies had found higher rates of GDM among African American women. However, subsequent studies controlling for maternal body mass index (BMI) have found little difference in incidence between African-Americans and Caucasians. DIAGNOSTIC EVALUATION The best time to screen for diabetes during pregnancy is at the end of the second trimester between 24 and 28 weeks' gestation in women with low risk for GDM. Patients with one or more risk factors for P.100 developing gestational diabetes should be screened at their first prenatal visit and, if negative, again in the early third trimester. TABLE 9-1 White Classification for Diabetes During Pregnancy ClassificationDescription Class A1 Gestational diabetes; diet controlled Class A2 Gestational diabetes; insulin controlled  Class B Onset: age 20 or older Duration: less than 10 years Class C Onset: age 10 to 19 Duration: 10 to 19 years Class D Onset: before age 10 Duration: greater than 20 years Class F Diabetic nephropathy Class R Proliferative retinopathy Class RF Retinopathy and nephropathy Class H Ischemic heart disease Class T Prior renal transplantation There are a variety of proposed methods of screening for diabetes during pregnancy (Table 9-2). In the United States, the most common laboratory screening test consists of giving a 50-g glucose load and then measuring the plasma glucose 1 hour later. If the 1-hour glucose level is greater than 130 or 140 mg/dL, then the test is considered positive and a glucose tolerance test, which often consists of a 100-g glucose load, is indicated. Recently, screening thresholds of 130 mg/dL or 135 mg/dL have been proposed that would increase the sensitivity of the test but at a cost of a larger proportion of women who will screen positive and thus need subsequent confirmatory testing. Thus, the optimal screen-positive threshold that maximizes sensitivity and costs is still under intense research and requires further elucidation. TABLE 9-2 Glucose Screening Tests During Pregnancy Test Normal Glucose Level (mg/dL) Fasting 38.3°C), abnormal cervical or vaginal mucopurulent discharge, abundant WBC on saline microscopy of vaginal secretions, elevated erythrocyte sedimentation rate, elevated C-reactive protein, and cervical Neisseria gonorrhoeae or Chlamydia trachomatis infection. Cervical cultures are performed to find a causative organism but, due to the disease's polymicrobial nature, should not dictate the treatment regimen. The definitive diagnosis is made via laparoscopy, endometrial biopsy, or pelvic imaging with PID findings. In practice, a more invasive diagnostic laparoscopic surgical procedure is usually performed only when appendicitis cannot be ruled out by clinical examination, although there are several small ongoing trials looking at the effectiveness of laparoscopy under local anesthesia for the diagnosis of PID. Occasionally, PID is complicated by Fitzhugh-Curtis syndrome (Color Plate 10). This is a perihepatitis from the ascending infection resulting in right upper quadrant pain and tenderness and liver function test (LFT) elevations. The principal organisms suspected of causing PID are N. gonorrhoeae and C. trachomatis; the two organisms combined account for approximately 40% of all PID cases. However, cultures from the upper reproductive tract have shown that most PID is likely to be polymicrobial, including anaerobic organisms such as Bacteroides species and facultative bacteria such as Gardnerella, Escherichia coli, H. influenzae, and streptococci. Treatment Because of the high rate of ambulatory treatment failures and the seriousness of sequelae, patients are often hospitalized for treatment of PID, particularly those who are teenagers, unable to tolerate POs, pregnant, noncompliant, or who have been refractory to outpatient therapy. PID is usually treated with a broad-spectrum cephalosporin, such as cefoxitin 2 g IV every 6 hours plus doxycycline 100 mg IV or orally every 12 hours because of its polymicrobial nature. The intravenous antibiotic regimen is continued until the patient demonstrates clinical improvement for 24 hours, and doxycycline is continued for a total 14-day course of doxycycline 100 mg orally twice a day. In patients allergic to cephalosporins, IV clindamycin and gentamicin can be used. On an outpatient basis, a single dose of ceftriaxone 250 mg IM or cefoxitin 2 g IM plus 1 g of probenecid orally along with oral doxycycline 100 mg orally twice a day for 14 days with or without metronidazole 500 mg orally twice a day for 14 days is used with close follow-up for resolution of symptoms. PID is rare in pregnant patients; because tetracyclines and fluoroquinolones are avoided in pregnancy, clindamycin and gentamicin is the treatment of choice during pregnancy. Additionally, due to increasing fluoroquinolone-resistant Neisseria gonorrhoeae in the United States, fluoroquinolones are no longer recommended by the CDC for treatment of gonorrhea infections or of PID cases in which gonorrhea may be a causative agent. TUBO-OVARIAN ABSCESS Persistent PID can lead to the development of tubo-ovarian abscess (TOA) (Fig. 17-2). Most so-called TOAs are actually tubo- ovarian complexes (TOC), the difference being that complexes are not walled off like the true abscess and are thus more responsive to antimicrobial therapy. Estimates of the progression from PID to TOA range from 3% to 16%; thus, any PID not responsive to therapy should be investigated further to rule out TOA. Furthermore, HIV-infected women with PID are at increased risk of development of TOA.  Figure 17-2 Findings associated with chronic pelvic inflammatory disease, including tubo-ovarian abscess, adhesions, pyosalpinx, and an abscess located in the posterior cul- de-sac. P.187 Diagnosis The diagnosis of TOA can be made clinically in the setting of PID and the appreciation of an adnexal or posterior cul-de-sac mass or fullness. Most patients will endorse abdominal and/or pelvic pain (90%) and demonstrate fever and leukocytosis (60% to 80%). WBC count is usually elevated with a left shift and the erythrocyte sedimentation rate (ESR) is often elevated as well. Cultures should include endocervical swabs and blood cultures to rule out sepsis. Culdocentesis that reveals gross pus is diagnostic but has been used less as advances in imaging studies have been made. Although most TOA are appreciated by clinical exam, a negative exam does not rule out a TOA. Ultrasound is the imaging study of choice to diagnose TOAs and is able to distinguish between TOAs and TOCs. However, pelvic computed tomography (CT) may be required, particularly in obese patients for whom ultrasound use is limited. Finally, laparoscopy can lead to a definitive diagnosis but is usually only used when the clinical picture is unclear. Treatment While treatment of TOAs can be medical or surgical, a trial of medical management with broad-spectrum antibiotics in an inpatient setting is frequently the first step. Unless the abscess is ruptured and causing peritoneal signs or is impenetrable by antibiotics, surgical treatment can often be avoided. The first-line antibiotic choice is often ampicillin (2 g IV every 4 hours), gentamicin (loading dose of 2 mg/kg, followed by 1.5 mg/kg IV every 8 hours or 5 mg/kg IV every 24 hours), plus clindamycin (900 mg every 8 hours) or metronidazole (500 mg PO or IV every 8 hours). In patients allergic to penicillin, ampicillin may be omitted. The course of this disease can be monitored by symptoms, clinical examination, temperature, WBC count, and, if these are equivocal, imaging studies. Typically, a repeat pelvic exam is performed after the patient has been afebrile for 24 to 48 hours to monitor for improvement and eventual resolution of tenderness. If responsive to medical management, the patient can be converted to oral antibiotics to complete a 10- to 14-day course. For more serious TOAs, either unresponsive to antibiotic therapy or with gross rupture, surgical intervention is necessary. Drainage of TOA using ultrasound guidance or laparoscopy may be considered in patients who do not respond to 48 hours of medical therapy. Unilateral salpingo-oophorectomy is considered as a curative therapy for the unilateral TOA by some authorities. For bilateral TOAs, often a total abdominal hysterectomy and bilateral salpingo-oophorectomy (TAHBSO) may be necessary. TOXIC SHOCK SYNDROME Toxic shock syndrome (TSS) reached its peak in the United States in 1980 when the rate was 3:100,000 menstruating women. Since 1984, there have been fewer than 300 cases per year. Initially, TSS was correlated with high-absorbency tampons and menstruation in approximately 50% to 70% of cases over the past two decades. Of note, the proportion of menstrual-related TSS has been decreasing over time. Nonmenstrually related TSS has been associated with vaginal infections, vaginal delivery, cesarean section, postpartum endometritis, miscarriage, and laser treatment of condylomata. Diagnosis TSS is caused by colonization or infection with specific strains of Staphylococcus aureus that produce an epidermal toxin— toxic shock syndrome toxin-1 (TSST-1). This toxin and other staphylococcal toxins are likely to cause most of the symptoms of TSS. Symptoms include high fever (>38.9°C or 102°F), hypotension, diffuse erythematous macular rash, desquamation of the palms and soles 1 to 2 weeks after the acute illness, and multisystem involvement of three or more organ systems. Gastrointestinal disturbances (abdominal pain, vomiting, and diarrhea), myalgias, mucous membrane hyperemia, increased blood urea nitrogen (BUN) and creatinine, platelet count less than 100,000, and alteration in consciousness can also be seen. Blood cultures are often negative, possibly because the exotoxin is absorbed through the vaginal mucosa. Treatment Because of the seriousness of the disease (2% to 8% mortality rate), hospitalization is always indicated. For more severe cases in which patients are hemodynamically unstable, admission to an intensive care unit may be necessary. Of highest priority is supportive treatment of hypotension with IV fluids and pressors if needed. Because this disease is caused by the exotoxin, treatment with IV antibiotics does not often P.188 shorten the length of the acute illness. However, it does decrease the risk of recurrence, which has been as high as 30% in women who continued to use high-absorbency tampons. Antibiotic therapy consists of clindamycin plus vancomycin for empiric treatment when specific S. aureus isolate sensitivity is unknown, clindamycin plus vancomycin or linezolid in MRSA TSS cases, and clindamycin plus nafcillin or oxacillin in MSSA TSS cases. Treatment duration is generally 10 to 14 days. Currently, there is a lack of controlled studies to support the use of intravenous immune globulin or corticosteroid therapy. HUMAN IMMUNODEFICIENCY VIRUS Human immunodeficiency virus (HIV) is the causative agent of acquired immunodeficiency syndrome (AIDS). HIV is transmitted via sexual contact, via parenteral inoculation, and vertically from mothers to infants via a transplacental route, during birth from direct exposure, and via breast milk. As of 2004, there were >123,000 cases of AIDS reported in girls and women in the United States. Although women account for only 18% of AIDS cases in the United States, they are one segment of the population in which the incidence is currently rising. The proportion of AIDS cases among female adults and adolescents (age >13 years) in the United States increased from 7% in 1985 to 27% in 2003. Furthermore, women of color (African American and Latina) have much higher infection rates compared to Caucasian women. More specifically, according to the CDC, African American women accounted for half of all HIV infection in men or women from heterosexual sex between 1999 and 2002. Worldwide, women represent a far more substantial proportion of those affected with HIV. According to the Joint United Nations Program on HIV/AIDS, in 2004, nearly 50% of adults living with HIV worldwide were women. In 2003, there were approximately 38 million patients with HIV, 3 million deaths due to HIV, and 1.1 million deaths directly attributed to HIV in women. There appear to be no differences in disease progression, mortality, or viral decay with use of antiretrovirals between men and women. Infection with HIV—a retrovirus—leads to decreased cellular immunity because various cells carrying the CD4 antigen become infected, including helper T cells, B cells, monocytes, and macrophages. Initially, the infection is entirely asymptomatic, although the individual is a carrier of the disease; this stage can last from 5 to 7 years. This disease may appear initially with the AIDS-related complex, which includes lymphadenopathy, night sweats, malaise, diarrhea, weight loss, and unusual recurrent infections such as oral candidiasis, varicella zoster, or herpes simplex. As the infection further decreases cellular immunity, full-blown AIDS develops with opportunistic infections such as Pneumocystis carinii pneumonia, toxoplasmosis, Mycobacterium avium intracellulare, cytomegalovirus, and various malignancies such as Kaposi sarcoma and non-Hodgkin lymphoma. Diagnosis The diagnosis of HIV infection is made initially via a screening test. Most commonly, the test is an enzyme-linked immunosorbent assay (ELISA) using HIV antigens, to which patient serum is added. A positive test results when antigen- antibody complexes form. This test does have false-positive results that, in low-risk populations, may occur more often than true positive results. Positive tests are therefore confirmed by a Western blot. Another level of confirmation may be obtained if a viral load is sent and is positive. Viral loads and CD4 cell counts are used to follow the progression of disease. Treatment There is no known cure for HIV or AIDS. The approach to this disease is prevention of transmission, prophylaxis of opportunistic infections, and prolonging the lives of infected patients by slowing progression of disease with antiretroviral agents. Great efforts are being directed toward prevention of HIV transmission by encouraging modification of risky behavior. Condoms are recommended for sexually active patients. IV drug users should avoid sharing needles and use clean needles. With improved screening methods, the risk of HIV infection from blood transfusion is currently estimated at less than 1:1,000,000. Prophylaxis and treatment of the opportunistic infections in HIV-positive patients are discussed in Blueprints Medicine. Delaying the progress of the disease is accomplished primarily with nucleoside analogs and protease inhibitors. The nucleoside analogs— zidovudine (AZT), lamivudine (3TC), abacavir, didanosine, and stavudine—act to inhibit reverse transcriptase and interfere with viral replication. Protease inhibitors (lopinavir, atazanavir, indinavir, saquinavir, ritonavir) interfere with the synthesis of viral particles and have been effective in increasing CD4 counts and P.189 decreasing viral load. Because the action mechanisms of these two groups differ, a synergistic effect is seen with combination therapy known as highly active antiretroviral therapy (HAART). Other antiretroviral drug classes include nonnucleoside reverse transcriptase inhibitors, and newer drug classes including entry inhibitors and integrase inhibitors. Beyond this simple review of HIV management, there are issues regarding HIV infection in women that deserve special emphasis. First, obstetric care of the HIV patient demands attention to both the ongoing care of the patient as well as the prevention of vertical transmission to the fetus. Second, the high incidence of invasive cervical cancer in this population requires more aggressive screening than in the general population. In the United States approximately 7,000 infants are born annually to mothers who are infected with human immunodeficiency virus. With no treatment, approximately 25% of infants born to HIV-infected mothers will become infected with HIV. Increased transmission can be seen with higher viral burden or advanced disease in the mother, rupture of the membranes, and invasive procedures during labor and delivery that increase neonatal exposure to maternal blood. Transmission occurs in utero (1/3) generally late in pregnancy or during labor and delivery (2/3). In 1994, Pediatric AIDS Clinical Trials Group (PACTG) protocol 076 demonstrated that a three-part regimen of zidovudine (ZDV) administered during pregnancy and labor and to the newborn could reduce the risk of perinatal transmission by two-thirds in women. Additionally, with the use of HAART to further decrease viral load with potent regimens, the rate of transmission can be further decreased to less than 1% to 2% with an undetectable viral load. Currently, antiretroviral therapy in pregnancy includes a three-drug regimen generally started in the second trimester with a goal for viral suppression by the third trimester, regardless of need for antiretrovirals for maternal health indication. Cesarean delivery has been shown to lower transmission rates by roughly two-thirds compared to vaginal delivery in patients on no therapy and particularly without onset of labor or rupture of membranes or in the setting of high viral load. However, in women with viral loads of 1,000 copies/mL and without long-standing onset of labor or rupture of membranes. Because of the effective interventions in HIV-positive women to decrease vertical transmission, it is recommended that HIV screening be offered to all pregnant women at their first prenatal visit and again in the third trimester if the woman has specified risk factors for HIV infection. Furthermore, in resource-rich nations where safe bottle feeding alternatives are available, breastfeeding is contraindicated in HIV-infected woman as virus is found in breast milk and is responsible for HIV transmission to the infant. Postnatal HIV transmission from breast milk at 2 years may be as high as 15%. Furthermore, studies are lacking regarding the efficacy of maternal antiretroviral therapy for prevention of transmission of HIV through breast milk and the toxicity of antiretroviral exposure of the infant via breast milk. The high incidence of invasive cervical cancer in HIV-infected women is an important issue in gynecologic outpatient management. Studies confirm the synergistic association of HIV and human papillomavirus (HPV), the causative agent in squamous cell carcinoma of the cervix. The Centers for Disease Control and Prevention currently recommends routine Pap smears at initial evaluation and 6 months later. Thereafter, yearly evaluations are sufficient if results are negative unless there is documentation of previous HPV infection, squamous intraepithelial lesion, or symptomatic HIV disease, in which case the Pap smear should be repeated at 6-month intervals. P.190 KEY POINTS Endomyometritis occurs most commonly after a delivery or instrumentation of the endometrial cavity. Diagnosis of endomyometritis is made with uterine tenderness, fever, and elevated WBC count. Endomyometritis treatment is with broad-spectrum antibiotics such as intravenous clindamycin and gentamicin; less severe infections are treated with intravenous cephalosporins. There may be as many as 1 million cases of PID reported annually. Twelve percent of patients with one episode of PID will become infertile. Minimal diagnosis criteria for PID consists of pelvic or lower abdominal pain, plus uterine, adnexal, or cervical motion tenderness. Because of the seriousness of this disease and its sequelae, patients are often hospitalized and treated with IV antibiotics. Chronic or acute PID can lead to TOAs or TOCs. Diagnosis of TOA or TOC is most likely when there is an adnexal mass in the setting of PID symptoms. Confirmation is usually achieved with an imaging study such as pelvic ultrasound or CT. TOA treatment includes hospitalization and broad-spectrum IV antibiotics. For TOAs not responsive to antibiotics, drainage of TOA is recommended. TSS peaked in 1984; currently, there are fewer than 300 cases per year in the United States. Symptoms, which include fever, rash, and desquamation of palms and soles, are most likely caused by an S. aureus toxin, TSST-1. Because of the seriousness of TSS, patients are hospitalized and treated with IV antibiotics and, if necessary, hemodynamic support. HIV is transmitted via sexual contact, sharing IV needles, and any activity where infected blood is introduced to a noninfected host. HIV infection is screened for with the ELISA test and confirmed with a Western blot. There is currently no cure for HIV infection so treatment focuses on antiretroviral agents such as nucleoside analogs and protease inhibitors and treatment of the multiple opportunistic infections. Vertical transmission rates during pregnancy have been shown to decrease with antiretroviral treatment and are positively associated with viral load. Chapter 18 Pelvic Organ Prolapse PELVIC ORGAN PROLAPSE PATHOGENESIS As shown in Figure 18-1, normal support of the pelvic organs is provided by a complex network of muscles (e.g., levator muscles), fascia (e.g., urogenital diaphragm, endopelvic fascia), nerves, and ligaments (e.g., uterosacral and cardinal ligaments). Damage to any one of these structures can potentially result in a weakening or loss of support to the pelvic organs (Fig. 18-2). Damage to the anterior vaginal wall can result in herniation of the bladder (cystocele) or urethra (urethrocele) into the vaginal lumen. Injuries to the endopelvic fascia of the rectovaginal septum can result in herniation of the rectum (rectocele) into the vaginal lumen. And injury or stretching of the cardinal ligaments and other pelvic support structures can result in descensus, or prolapse, of the uterus (uterine prolapse). After hysterectomy, some women may experience prolapse of the small intestine (enterocele) or vagina secondary to loss of support structures during surgery (vaginal vault prolapse). Pelvic organ prolapse can present with a variety of symptoms including pelvic pressure and pain, urinary incontinence, dyspareunia, and bowel and bladder dysfunction. Pelvic support can be compromised by birth trauma; chronic increases in intra-abdominal pressure from obesity, chronic cough, or heavy lifting; intrinsic weakness; and atrophic changes due to aging or estrogen deficiency. Pelvic organ prolapse quantitative (POP-Q) refers to an objective, site-specific system for describing, quantifying, and staging pelvic support in women. It provides a standardized means for documenting, comparing, and communicating clinical findings of pelvic organ prolapse that focuses on the extent of prolapse and not on which organ part is presumed to be prolapsing within the defect (Fig. 18-3). In order to quantitatively assess the degree of prolapse involved, POP-Q uses six points within the pelvis that are measured in relation to a fixed point of reference: the hymen. POP-Q is not used uniformly by clinicians because it is quite complicated, but it is helpful in the research setting and in comparing patients' exams over time and among different examiners. Most clinicians utilize the Baden-Walker Halfway System for quantifying pelvic organ prolapse. It records the extent of prolapse using a four-point system using the hymen as a fixed point of reference (Fig. 18-4). Zero represents normal anatomic position (i.e., no descensus), 1: descensus halfway to the hymen, 2: descensus to the hymen, 3: descensus halfway past the hymen, and 4: maximum descent. The examination is usually conducted with the patient straining in order to record maximum descent. EPIDEMIOLOGY The problem of pelvic relaxation is increased in postmenopausal women secondary to decreased endogenous estrogen and increased vaginal deliveries. As a result, tissues become less resilient and the accumulative stresses on the pelvis take effect. Black and Asian women have a much lower rate of uterine prolapse than do white women. P.192 Figure 18-1 Normal structural support of the pelvic floor as seen from above. Figure 18-2 Anatomic defects in pelvic relaxation. Figure 18-3 Schematic of the quantified pelvic organ prolapse (POP-Q) system. Six sites (points Aa, Ba, C, D, Bp, Ap), genital hiatus (gh), perineal body (pb), and total vaginal length (tvl) are used to quantify the degree of pelvic organ prolapse. The vagina and hymenal ring are shown in blue. P.193  Figure 18-4 Baden-Walker halfway system for grading pelvic organ prolapse. In general, grade 1 is given to a defect which descends at least halfway to the hymenal ring. Grade 2 is given to a defect extending to the hymenal ring. Grade 3 is given to a defect extending half-way beyond the hymenal ring. Grade 4 is given if the uterus is completely outside of the vagina. (Image from Rock J & Jones H. TeLinde's Operative Gynecology, 10th ed. Philadelphia: Lippincott Williams & Wilkins, 2008.) RISK FACTORS The incidence of pelvic relaxation is increased for those patients who have chronically increased abdominal pressure due to chronic cough, chronic constipation, repeated heavy lifting, and large pelvic tumors. Obstructed labor and traumatic delivery are also risk factors for pelvic relaxation as are aging and menopause. CLINICAL MANIFESTATIONS History The symptoms reported with pelvic relaxation vary depending on the structures involved and the degree of prolapse (Table 18- 1). With small degrees of pelvic relaxation, patients are often asymptomatic. With more extensive relaxation, patients often complain of pelvic pressure, heaviness in the lower abdomen, or a vaginal bulge that may worsen at night or become aggravated by prolonged standing, vigorous activity, or lifting heavy objects. Urinary incontinence, frequency, urgency, and retention are other symptoms that may also be reported by patients with pelvic organ prolapse. Physical Examination Pelvic relaxation is best observed by separating the labia and viewing the vagina while the patient strains or coughs. A split- speculum exam can also be performed by using a Sims speculum or the lower half of a Grave speculum to provide better visualization of the anterior and posterior vaginal walls individually. Using this method, the speculum is used to retract the posterior vaginal wall and a cystocele may cause a downward movement of the anterior vaginal wall when the patient strains (Fig. 18-5). Similarly, rectoceles and enteroceles result in an upward bulging of the posterior vaginal wall when the patient strains (Fig. 18-6). This laxity in the rectovaginal wall can P.194 also be demonstrated on rectal exam. A prolapsed uterus can also be viewed on split-speculum examination or by bimanual pelvic exam. TABLE 18-1 Symptoms That May Be Manifested in Pelvic Organ Prolapse Pressure Symptoms Other Urinary Symptoms Pelvic pressure or heaviness Frequency hesitancy Backache Incomplete voiding Dyspareunia Recurrent infection Urinary incontinence Rectal symptoms Constipation Painful defecation Incomplete defecation Splinting * * Placement of the fingers in the vagina to aid in defecation.  Figure 18-5 A cystocele (seen here via split-speculum exam) is the bulging of the bladder into the anterior vaginal wall. It is usually caused by pelvic floor weakness. It can be repaired with an anterior colporrhaphy. The degree of pelvic relaxation is determined by the amount of descent of the structure. In first-degree pelvic relaxation, the structure is in the upper two-thirds of the vagina. In second-degree pelvic relaxation, the structure descends to the level of the introitus. In third-degree pelvic relaxation, the structure protrudes outside of the vagina. In fourth-degree pelvic relaxation, the entire structure is outside the vagina (Color Plate 11). DIAGNOSTIC EVALUATION The diagnosis of pelvic organ prolapse depends primarily on the history and physical examination. Other tools that may be useful in the diagnosis and preoperative evaluation of cystoceles and urethroceles include urine cultures, cystoscopy, urethroscopy, and urodynamic studies, if indicated. When a rectocele is suspected from a history of chronic constipation and difficulty passing stool, obstructive lesions should be ruled out using anoscopy or sigmoidoscopy. A defecography study (similar to a barium enema) may also help to show a rectocele or enterocele but is not generally essential to diagnosis. DIFFERENTIAL DIAGNOSIS Although rare, the differential diagnosis for cystocele and urethrocele includes urethral diverticula, Gartner cysts, Skene gland cysts, and tumors of the urethra and bladder. When a rectocele is suspected, obstructive lesions of the colon and rectum (lipomas, fibromas, sarcomas) should be investigated. Cervical elongation, prolapsed cervical polyp, and prolapsed cervical and endometrial tumors may be mistaken for uterine prolapse as can lower uterine segment fibroids. TREATMENT Regardless of the etiology, symptomatic pelvic organ prolapse is essentially a structural problem and therefore requires therapies that reinforce the lost support to the pelvis. These structural remedies may include hormonal therapies to maximize intrinsic pelvic support or exercises to strengthen the pelvic musculature (Kegel exercises). Likewise, mechanical support P.195 devices (pessaries) may be used or the defect may be repaired surgically. Figure 18-6 A rectocele is the bulging of the rectum into the posterior vaginal wall. It is  usually caused by pelvic floor weakness. It can be repaired with a posterior colporrhaphy. In postmenopausal women, estrogen replacement (systemic or vaginal) can be an important supplemental treatment, improving tissue tone and facilitating reversal of atrophic changes in the vaginal mucosa. In motivated patients with mild symptoms, a first attempt at treatment may involve the use of Kegel exercises to strengthen the pelvic musculature. These exercises involve the tightening and releasing of the pubococcygeus muscles repeatedly throughout the day to strengthen the muscles and increase pelvic support. Vaginal pessaries act as mechanical support devices to replace the lost structural integrity of the pelvis and to diffuse the forces of descent over a wider area. Pessaries are indicated for patients in whom surgery is contraindicated but whose symptoms are severe enough to require treatment. These are used in pregnant and postpartum women as well. These devices are placed in the vagina, positioned like a diaphragm, and serve to hold the pelvic organs in their normal position (Fig. 18-7). The use of vaginal pessaries requires a highly motivated patient and close clinical follow-up to avoid vaginal trauma and ulcerations. Close follow-up also ensures proper placement and hygiene to minimize the risk of leukorrhea and infections. Symptomatic patients who are not helped by nonoperative approaches may require surgical correction. In general, surgical repair for pelvic relaxation produces very good results. As outlined in Table 18-2, correction of cystoceles and rectoceles can be accomplished by anterior and posterior colporrhaphy, respectively. These procedures repair the fascial defect through which the herniation occurred (see Figs. 18-8, 18-9, and 18-10). Enteroceles, which represent the herniation of small bowel into the vaginal canal, can be repaired along with the reinforcement of the rectovaginal fascia and the posterior vaginal wall. With significant uterine prolapse, abdominal or vaginal hysterectomy may be indicated. In women who have prolapse of the vaginal vault after hysterectomy the vaginal vault prolapse is corrected by suspension of the vaginal apex to fixed points within the pelvis such as the sacrum (abdominal sacral colpopexy) or sacrospinous ligaments (sacrospinous ligament fixation). The degree of success depends on the skill of the surgeon, the degree of pelvic relaxation, and the age, weight, and lifestyle of the patient. Figure 18