Obstetrics and Gynecology at a Glance ERROL R. NORWITZ, MD, PhD Harvard Medel School vf Maternal eta! Medicine Department of Obstetries and Gynecology Brigham & Women's Hospital Boston MA, USA JOHN O. SCHORGE, MD Assistant Professor Division of Gynecologic Oncology Department of Obstetries and Gynecology The University of Texas Southwestern Medical Center Dallas TX, USA b Blackwell ScienceOsney Mead, Oxford OX2 061. 235 Jol Street, London WCIN 23 Atal Phce, Edinburgh EHS 6A 380 Main Street, Malden MA 02188-9018, USA, $4 University Street, Cashion Victoria MS. Australia 10, rue Case Delage "soon Par France Other Ediorial Ofices: Blackwell Winenschae Verlag GmbH Kuatsteedamm $7 10707 Bevin, Germany Blackwell Science KK. 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Commerce Pace 4350 Main Street, Malden, MA 0214801 (Onder Tek: 007896102 781 ROS) Fa 78 88 ADSS) Canada ‘Login Brothers Book Company 2324 Sauenux Crescent ‘winnipeg. Manitoba RY 372 (Onder Tek 208887 987) Ate Blackwell Science Pay Lad 54 University Sect ‘Carhon, Vitora M3 (Onder Tet 39347 0340 Fax: 39397 0) A catalogue coed for this tie ‘aval from the British Library ISBNO-A2ONEIS Library of Congress (Catalopingin-Pubicaton Data [Norwitz rot R, ‘Obstctnes and gynecology at glance / Erna R. Nori, John O, Sehorge poem Ince bibliographical references and index ISBN Oss2-08510 1. Obstetrics Handbooks, manuals, ete. 2. Gynccology-Handhook, manuals ete 1 Schorge. John OU. Ti [DNLM: 1. Genital Diseases, Female-Handbooks. 2. Genital Noo plasm. Female-Handbooks. 3. Pregnancy Complications-Handbooks. WP Jy NNO 3] RGHO.N6? 2001 618-421 wosesi0 For anther formation on [Bucknell Scteae, iit our website: ‘enw blackell secre somContents Preface 4 Acknowledgements 5 Further reading $ Table and figure acknowledgements 6 Part 1: Gynecology 1 Anatomy of the female reproductive tract 8 2 The menstrual cycle 10 3 Abnormal vaginal bleeding, 12 4 Ectopie pregnaney 14 5 Pelvie pain 16 6 Infections of the lower genital tract 18 7. Pelvic inflammatory disease 20 8 Gynecologic surgery 22 9 Benign disorders of the lower genital tract 24 10. Benign disorders of the upper genital tract 26 11 Endometriosis and adenomyosis 28 12 Contraception 30 13. Sterilization 32 14 Urinary incontinence and genital prolapse 34 Part 2: Reproductive endocrinology and infertility 15 Puberty and precocious puberty 36 16 Amenorrhea 38 17 Polycystic ovarian syndrome 40 18 Hirsutism and virilization 42 19. Abortion 44 20. Recurrent pregnancy loss 46 21 Antiphospholipid antibody syndrome 48 22 Cervical incompetence and cervical cerclage SO 23. The infertile couple 52 24 Ovulation induction 54 25 Assisted reproductive technology 56 26 Menopause and hormone replacement therapy 58 Part 3: Gynecologic oncology 27 Ovarian cancer 60 28 Uterine cancer 62 29. Cervical cancer 64 30 Vaginal and vulvar eancer 66 31 2 3 ‘Other gynecologic malignancies 68 Gestational trophoblastic disease 70 Chemotherapy and radiotherapy 72 Part 4: Obstetrics ey 35 36 37 38 39 40 41 2 8 45 46 47 48 49 50 3 2 33 34 $5 56 7 38 39 0 61 @ 6 64 65 66 Embryology and early fetal development 74 Fetal physiology 76 Endocrinology of pregnancy and parturition 78 Maternal adaptations to pregnancy 80 Prenatal diagnosis $2 ‘Obstetric ultrasound 84 Infections in pregnancy: bacteria and protozoa 86 Infections in pregnancy: viruses and spirochetes 88 Hypertensive disorders of pregnancy 90 Diabetes mellitus in pregnancy 92 Cardiovascular disease in pregnancy 94 ‘Thyroid discase in pregnancy 96 Other medical and surgical conditions in pregnancy 98 Drugs and medications during pregnancy 100 Disorders of amniotic uid volume 102 Disorders of fetal growth 104 Antepartum fetal surveillance 106 Hydrops fetalis 108 Intrauterine fetal demise 110 Multiple pregnancy 112 Antepartum hemorrhage 114 Premature labor 116 Premature rupture of the membranes 118 Induction and augmentation of labor 120 Normal labor and delivery 122 Abnormal labor and delivery 124 Pain relief in labor 126 Intrapartum fetal monitoring 128 Operative vaginal delivery 130 Cesarean delivery 132 Third stage of labor and postpartum hemorrhage 134 ‘The puerperium 136 ircumcision 138Preface ‘The medical and scientitic problems of this world eannot be solved by skeptics whose horizons are limited by practical realities We need women and men who dream of things that ‘cannot be and ask why not Professor Egon Diczfalusy, Karolinska Institute, Stockholm, Sweden, 1992 Medicine continues to attract the brightest and most dedicated students to its ranks. The opportunity to nurture the talented ‘young minds that will one day rise up to lead the medical com- ‘munity remains the single greatest privilege for the academic linician. Nowhere is this privilege—and challenge—more appar- ‘ent than in obstetrics and gynecology, a discipline that remains more art than science. Although clinicians in all disciplines aspire to practice rational evidence-based medicine, many basic ques- tions in the field of obstetrics and gynecology remain unan- swered. While cardiologists measure changes in calcium flux ‘within a single myocardial cell and nephrokogists estimate changes in osmotic gradient along a single nephron, obstetri- langynecollogists continue to. debate such questions as: How is the LH surge regulated? What causes endometriosis? Why is there still no effective screening test for ovarian cancer? What triggers labor? ‘This book is written primarily for medical students starting their clinical rotations. Itis designed to give the reader a succinct Yet comprehensive review of obstetrics and gynecology. Each Chapter consists of two pages: page of text and an accompanying set of images or algorithms that serve fo compliment the text. lis the sincere hope of the authors that the reader will find this book Interesting, easy to read, and informative, Not all questions.can be answered in a formal text format. Students should be encouraged to question and challenge their clinical teachers. Only then can the fleld move forward, Remember: “We need women and men who dream of things that cannot be and ask why not Erol R, Norwitz, MD, PhD John O. Schorge. MDErrata Leader lines are missing from Figs 1, 5, 45 and 48. The corrected parts are shown below. THE VULVA Fig. Fig. DIAGNOSIS OF MATERNAL THYROID DYSFUNCTION IN PREGNANCY, Hyperthyroiaen Hypothroidion Peychome myedera mmadnees!), coma, cold Intceronce, tellectua litation ae nem, 1H, fasta 4 \ cholesterol mug Ee ‘cure eee ea face, large tongue) — monies bree nat P Thyromegaly- consamegay ede Mere poreeraal oer, tim ebees ‘tety rere Modes ne Frets mater 4. eon omepaion Trenosrese ‘ine veror neenreses Pate, coo thi dey kn ie ‘ation pase) EMBRYOLOGY OF THE AMNIOTIC CAVITY cockom bed Norwite & Schorge: Obstetrics and Gynecology ata Glance. Blackwell Science 2001Acknowledgements 1 would like to thank my wife, Ann; my parents, Rollo and Marionne: and my children, Nicholas, Gabriella, and Sam for all their support. Errol R. Norwitz, MD. PRD. Further reading Creasy RK. (ed) (1997) Management of Labor and Delivery. Blackwell Science, Malden, DiSaia PL & Creasman WT. (eds) (1997) Clinical Gynecolosic Oncology, 5th edn. Mosby-Year Book Inc..St. Louis, Missouri. Gabbe SG, Niebyl LR. & Simpson LL. (1996) Ohstetrice: Normal ‘and Abnormal Pregnancy, Xd edn. Churchill Livingstone. New York. Mishell D.R.,Stenchever M.A. & Droegenmaller W. (eds) (1997) Comprehensive Gynecology, 3rd edn, Mosby-Year Book Ine. St. Louis Missouri would like to thank my wife Sharon and deg Kramer for their support during the completion of this book. In addition, I would like to express my deep appreciation for the faculty who inspired ‘me during my obstettics and gynecology training—most notably John Repke, Ellen Sheets, Ross Berkowitz and Sam Mok. John O. Schorge. MD Reece E.A, & Hobbine J.C. (eds) (1999) Medicine of the Fes ‘and Mother, 2nd eda. Lippincott-Raven, Philadelphia. Repke JT: (ed) (1996) Intrapartum Obstetrics, Churchill Living: ‘stone, New York. Rock LA. & Thompson ID. (eds) (1997) TeLinde’s Operative Gynecology. 8th can, Lippincott-Raven, Philadelphia. Speroff L.. Glass RH. & Kase NG, (eds) (1999) Clinical Gynecologic Endocrinology and tafertilty, 6th ed. Williams & ‘Wilkins, Baltimore, Maryland,Table and figure acknowledgements ‘The following tables and figures have been redrawn from the originals and were used with permission of the publishers. Every effort hhas been made by the author and the publishers to contact all the copyright holders to obtain their permission to reproduce copyright material. However the frst opportunity. 1 Anatomy of the female reproductive tract Parts of the figure redravin with permission from: Morrow. CP & Curtain, LP. (1996) Gynecologic Cancer Surgery, 115. Churchill Livingstone, London. 4 Fetopie pregnancy “Table redrawn with permission from: ‘The American College of Obstetricians and Gynecologists. (1998) Medical managemen’ of ubal pregnancy. ACOG pace Lice bulletin No. 3, Washington DC. 8 Gynecologic surgery Paris of the figure redrawn with permission from: Whecless. CR. (1997) Atlas of Pelvie Surgery, Sed edn, p.263. Lip- pincott, Williams & Wilkins, Philidelphia 9 Benign disorders of the lower genital tract Parts of the figure redrawn with permission from: Netter. FH. (1992) The Reproductive System. In: The CBA Col- lection of Medical tMtusirarions, Vol 2, 9h edn, pp.140 & 151 ICON, New Jersey. 10 Benign disorders of the upper genital tract Paris ofthe figure redrawn with permission from: DiSoia, PL Creasman, WT (1997). Clinical Gynecologic Oneol- ‘ogy, Sth edn, pp. 180 & 261. Mosby, St. Louis. Netter. FH. (1992) The Reproductive System. In: The CIBA Ce lection of Medical ttusirations, Vol 2, 9th edn, p. 201. ICO? New Jersey. LI Endometriosis and adenomyosis Parts of the figure redrawn with permission from: Ryan, K1, Berkowitr, RS. & Barbieri, R.L. (1995) Kistner’ ‘Gynecology : Principles and Practice. 6th edn, p. 254, Mosby. St Louis 13 Sterilization Parts of the figure redrawn with permission from: Speroff, L, Glass, R-H. & Kase, NG. (1994) Clinical gynecologic ‘endocrinology and inferiliy, Sth edn, pp. 695-697. Lippincott, Williams & Wilkins Philadelphia. 15 Puberty and precocious puberty Parts of the figure redrawn with permission from: Sperofl L.. Glass, RH. & Kase, NG. (1994) Clinical gynecologic ‘endocrinology and infertility, Sth edn, pp. 378-379. Lippines Williams & Wilkins, Philadelphia. any have been inadvertently overlooked, the publisher wil be pleased to make the necessary arrangements at 16 Amenorrhea Parts of the figure redrawn with permission from: Netter, FH. (1992) The Reproductive System. In: The CIBA Col- lection of Medical Mustracions, Vot 2, 9th edn. p. 193. ICON, New Jersey. 25 Assisted reproductive technology Parts of the figure redrawn with permission from: Gershenson, D.M.. DeCherney. A.H. & Curry, SL. (1993) Oper- ative Gynecology, pp. S57-S64. W.B, Saunders, Philadelphia. 33 Chemotherapy and radiotherapy Parts of the figure redrawn with permission from: DiSaia, PJ.& Creasman,W.T. (1997) Clinical Gynecologic Oncol- ogy, Sth eda, p 514, Mosby, St. Louis, 3M Embryology und early fetal development Parts of the figure redrawn with permission from: Moore, K.L, (1988) The Developing Human: Clinically Orientated Embryology, 4th edn. W.B. Saunders, Philadelphia. Moore, K.L. & Persaud, LVN. (1993) The Developing Human, Clinically Oriemtated Embryology, Sth edn. WB. Saunders, Philadelphia, AS Fetal physiology Parts of the figure redrawn with permission from: Brown,A.R,& Assali, NS. (1968) The Fenus and Neonate, Biology of Gestation. p31. Acadernic Press, New York Fox, H. & Elston, CW, (1978) Pathology of the Placenta. WB. ‘Saunders, Philadelphia, 36 Endocrinology of pregnancy and parturition Parts of the figure redrawn with permission from: Norwitz, E:R., Robinson, LN. & Repke, 1:1. (1999) The initiation ‘of parturition: a comparative analysis across the species. Current Problems in Obsteirics and Gynecology and Ferility, 22, 41-72 37 Maternal adaptations t0 pregnancy Pants ofthe figure redrawn with permission from: Leontic. E.A, (1977) Respiratory disease in pregnancy. The ‘Medical Clinics of North America, 61, U4. Scot, DIE. (1972) Anemia during pregnancy. Obstewies and Gynecology Annual 1,219,‘Table redrawn with permission from: Clark, SL., Cotton, D.B., Lee, W.. Bishop, C. & Hill, T, (1989) Central hemodynamic assesment of normal-term pregnancy. American Journal of Obstetrics and Gynecology, 161, 1439. 38 Prenatal diagnosis Parts of the figure redrawn with permission from: ‘Wald, N.& Cuckle, HS. (1987) Recent advances in screening for neural tube defects, Bailleres Clinical Obstetrics and Gynae- cology, 1, 656. ‘Table redrawn with permission from: Patient education bulletin. (1994) Maternal serum screening for bik defeets. No. APOS9, American College of Obstetrics & Gynecology, Washington DC. 39 Obstetric wtrasound Paris of the figure redrawn with permission from: Romero, R., Plu, G. Jeanty, P, Ghidini, A. & Hobbins J.C. (1998) Prenatal Diagnosis of Congenital Anomalies, pp. 128-129. Appleton & Lange, New York. 45 Thyroid disease in pregnancy Parts of the figure redrawn with permission from: Fisher, D.A. & Carson, PR. (1994) Maternal and fetal thyroid functin. New England! Journal of Medicine, 331 (Suppl, 16), 1072-1078, ‘53 Multiple pregnancy Parts of the figure redrawn with permission from: Norwitz, E.R. (1998) Multiple pregnancy: trends past, present and future. Infertility and Reproductive Medicine Clinics of North America, 9 (Suppl. 3) 351-69, ‘55 Premature labor Parts of the figure redrawn with permission from: Norwitz, E.R., Robinson, IN, & Repke, T. (1999) The initiation ‘of parturition: comparative analysis across the species Current Problems in Obsteiics and Gynecology and Ferlity, 22 (Suppl. 2), 41-72. ‘Table redrawn with permission from: Norwitz, E.R., Robinson, JN.& Challis, LRG. (1999) The control of labor. The New England Journal of Medicine, 381 (Suppl. 9), 664, [58 Normal labor and delivery Friedman, E.A. (1978) Labor: Clinical Evaluatin and Manage ‘ment, 2nd edn. Appleton-Century-Crafts New York Norwitz, E.R., Robinson, JN. & Repke, £7, The initiation and ‘management of normal labor. In: The Physiologic Basis of mnecology and Obstetrics. (eds. DIB. Seifer, P. Samuels & D.A. Kniss) p. 422. Lippincott, Williams & Wilkins, Philadel- phia.Anatomy of the female reproductive tract THE VULVA PELVIC FLOOR MUSCULATURE Sopot perneal compartment Pee aaphrapm . “a |\ sas ge, | Sees w# Vestine refectod Sas acces Tana fae INTERNAL GENITALIA otorinus Recwes mace revected 8 Gynecology‘The vulva and pelvic floor musculature + The vulva is the visible external female genitalia bounded by the mons pubis anteriorly, the anus posteriorly. and the genito- ‘rural folds laterally. * The perineum is located between the urethral meatus and the anus, ineluding both the skin and the underlying muscle + The mons pubis consists of hair-bearing skin over 2 cushion of adipose tissue that lies on the symphysis pubis © The labia majora are two large, hait-bearing cutaneous folds of adipose and fibrous tissue extending from the mons pubis to the perineal body * The clitoris is short, erectile organ with a visible glans It is the female homologue of the male penis. + The labia minora are two thin, haitless skin folds medial to the labia majora which originate at the clitoris ‘© The vestibule isthe cleft of tissue between the labia minora that is visualized when they are held apart * Bartholin' glands are situated at each side of the vaginal orifice with duct openings at 5 and 7 o'clock. © The superficial perineal comparment is located between Colles’ fascia and the urogenital diaphragm. Within it are found the ischiocavernosus, bulbocavernosus.and superficial transverse perineal muscles. # The urogenital diaphragm (perineal membrane) is 9 wiangular sheet of dense, fibromuscular tissue stretched between the sym- pphysis pubis and ischial tuberosities in the anterior half of the pelvic outlet. I's primary funetion is to support the vagina and perineal body. * The pelvic diaphragm is found above the urogenital diaphragm and forms the inferior border of the abdominopelvic cavity. It is ‘composed of a funnel-shaped sling of fascia and muscle (levator ani, coceygeus) Internal genitalia and lateral pelvic anatomy + The werus isa fibromuscular organ whose shape, weight, and dimensions vary considerably. The dome shaped top is termed the fundus. + The cervir is connected to the uterus atthe internal ox Is made up primarily of dense fibrous connective tissve. The cerv cal canal opens into the vagina atthe external os. + The wagina sa thin-walled, distensible fibromuscular tube that extends from the vestibule of the vulva to the uterine cervix. © The fallopion wubes (oviducts) are paired tubular structures that arise from the upper lateral portion ofthe uterus, widening iin their distal third (ampulla). * The ovaries are whiish-gey,almond-sized organs attached 10 the uterus medially by the utero-ovarian ligaments and 10 the pelvic sidewall laterally by a vascular pedicle, the infundibulo- pelvie ligament The urewers are whitish, muscular tubes which serve as a conduit for urine from the kidney to the bladder trigone. They sourse over the common iias vesels from lateral to medial at the level of the pelvic brim before passing under the uterine vessel just lateral to the cervix (water under the bridge’) * The bladder is hollow muscular organ that lies between the symphysis pubis and the uterus. The size and shape varies withthe volume of urine © The sigmoid cofon enters the pelvis on the left, forming the rectum at the level of the second and third sacral vertebrae, and ‘ending at the anal canal = The round ligaments are paired fibrous bands that originate at the uterine fundus and exit the pelvis through the internal inguinal ring. They provide litle structural support. © The brow! ligamems are thin reflections of the peritoneum stretching from the pelvie sidewalls to the uterus. They provide Virtually no suspensory support, but are draped over the fallop- jan tubes, ovaries, round ligaments, ureters, and other pelvic structures © The cardinal (Mackenrodt’s) ligaments provide the major ‘support of the uterus and cervix. They extend from the lateral aspects of the cervix and vagina 10 the pelvie sidewalls = The ulerosacral ligaments serve a minor role in the anatomic ‘support of the cervix, They extend from the upper cervix poste- riorly to the third sacral vertebra ‘Arterial blood supply of the pelvis ‘© The aorta bifurcates at the fourth lumbar vertebra to form the {two common iliac arteries which in turn divide to form the exter- nal iliac and hypogastric (internal iliac) arteries, ‘© The external iliac artery passes under the inguinal ligament to become the femoral artery: ‘ The hypogastric artery branches into anterior and posterior visions to supply the pelvis. ‘© The ovarian arteries originate from the infrarenal aorta and reach the ovaries via the infundibulopelvi ligament. ‘= The inferior mesenteric artery arises from the aorta, 3em above the bifureation, to supply the descending colon. ‘ The internal pudendal artery supplies the rectum, labia. clitoris, and perineum. Innervation of the genital tract * The innervation of the internal genital organs is supplied by the autonomic nervous system, chiefly via the superior Bypogas- tric plexus * The pudendal nerve arises from the sacral plexus and courses with the pudendal artery and vein through the pudendal (Aleock’s) canal to supply both motor and sensory fibers to the muscles and skin of the perineum. Lymphatic drainage + The vulva and distal third of the vagina are supplied by an anastomotic series of lymphatic channels which coalesce to drain primarily into the superficial inguinal nodes. ‘= Lymphatic drainage of the upper two thitds of the vagina and uterus is primarily to the obturator, external iliac, and hypogas- trie nodes. ‘© The lymphatic drainage ofthe ovary follows the ovarian vessels to the paraaortic mph nodes. ‘Abdominal wall Layers of the abominal wall include~from the outside to the inside—the skin, subewianeous layer (Scarpa's fascia), musculo- ‘qponeurotic layer (rectus sheath, external oblique muscle, inter: nal oblique muscle, ransversus abdominis muscle), ransversalis fascia, and peritoneum (opposite). Anatomy of the female reproduetive tract 92 The menstrual cycle HORMONAL REGULATION OF OVULATION : ‘rum eSSSERE | : 0 0CEGe Maroon foley Connon sm | Eotradioh 7B Ho" ‘Steroid mutes Hs : (cyclopentenophenanthrene) ¢=o i i} Ei ; oS o Vena Fraeeaine __ eal fase | phase + (ecretery phase Putsate GrRM Negative feedback Gonadocropine e ‘Anterior pituitary | PY Steroid hormones, aH i Gamerooenesio, (development of cocyte) and onistion (cotradioM47B, progesterone) 10 GynecoogyDefinitions ‘© Menstruation refers to the eyelic uterine bleeding experienced ‘by most women of reproductive age, ‘© Menarche the onset of menstruation) o ‘of 12 years (normal range, $-16 years), * Puberty isa general term encompassing the entire transitional stage from childhood to sexual maturity. + Ovulatory menstrual cycles usually last between 24 and 35 days (average, 28 days). «© The average duration of menstruation is 3-7 days ‘© The average menstrual blood loxs is 80 mL. ‘© The average age of menopause (menstrual cessation) is $1 wurst an average age ‘Hormonal regulation of ovulation ‘The eyclopentenophenanthrene ring structure isthe basie carbon skeleton for all steroid hormones. Cholesterol is the parent steroid from which all the glucocorticoids, mineralcorticoids, and ‘zonadal steroids are derived, Phases of the menstrual cycle (opposite) ‘ The first day of menstruation is defined as day 1 of the men: strual eyele. ‘© The mensirual phase refers to the period of shedding of the wlometsial ining. ‘+ The proliferative phase of the menstrual eyele begins at the end fof the menstrual phase (usually day 4) and ends at ovulation (usually day 13 oF 14).This phase is characterized by endometrial thickening and ovarian follicular maturation. © The lmiinizing hormone (LH) surge on day ‘ovulation, * The luteal (sceretory) phase starts at ovulation and lasts through day 28 of the menstrual eycle, The corpus luteum devel- ‘ops to synthesize steroid hormones. or 14 triggers Biologic basis of menstruation ‘Coordination of the menstrual eycle depends on a complex inter- action between the brain, the pituitary, the ovaries, and the endometrium. Brain * The hypothalamus acts as a transducer to convert neuronal stimuli from the cerebral cortex into pulses of neuropeptides, ‘which travel to the anterior pituitary. + Hypothalamic production of neuropeptides, such as ‘gonadotropin-releasing hormone (GaRH), is modulated by eg- lative feedback of steroid hormones. Pimitary ‘Pulsatile GaRH from the hypothalamus initiates the synthes ‘and secretion of the pituitary gonadotropin, LH and follick stimulating hormone (FSH). * LH and PSH production is also subject regulation by the steroid hormones. * In reproductive age women, LH and FSH levels generally remain in the 10-20miL/mL. range. After the menopause or ‘oophorectomy, estradiol-17B levels decline and pituitary gon- adotropins are released from negative feedback, achieving circulating concentrations of more than SO mIU/mL. negative feedback Ovaries * Primitive germ cells (oogonia) divide by mitosis during fetal ‘embryogenesis, peaking at around 7 million by 5 months of ‘gestation, ‘+ Meiotic division then begins resulting in formation of primary oocytes, However, rapid atresia reduces the number of available follicles to 2 million at birth, At puberty. only around 300000 400000 follicles remain. = Oocytes remain ‘resting’ in meiotic prophase until puberty Resting ovarian follicles are surrounded by thecal and granulosa cells; FSH stimulates the granulosa cells and LH stimulates the theea cells. # Only asingle*dominant follicle’ develops each menstrual eycle. When it produces enough estrogen 10 sustain a circulating cstradiol-178 concentration of approximately 200 pa'mL. for 48h, the hypothalamic-pituitary axis responds by secreting a surge of gonadotropins, primarily LH. This Lif surge precedes ovulation by 24-36h, + Following ovulation, the follicle collapses to form the corpus Iuscum. This endocrine organ mainly synthesizes progesterone to prepare the endometrium for pregnancy. ‘© If implantation does not occur the corpus luteum will degenerate, resulting in a precipitous decline in circulating steroid hormone levels and the onset of menstruation, The decreasing steroid hormone levels release the negative feedback mechanism, inducing the pituitary to increase gonadotropin secretion. As a result, a new cycle of follicular recruitment is initiated, ‘= If implantation does occur, the embryo will rescue the corpus luteum by producing human chorionic gonadotropin (hCG) to prevent menstruation, At 7-9 weeks of gestation, the placenta takes over the production of progesterone from the corpus futeum, Endometrium ‘© Estradiol-I7B production by the ovarian follicles induces endometrial proliferation. Progesterone synthesis by the corpus luteum then acts to mature the estrogen-primed endometrium in preparation for blastocyst implantation. # Lowered steroid hormone levels in the late secretory phase cause a collapse of the endometrial vasculature, resulting in menstruation. Premenstrual syndrome (PMS) *# Defined 4s the cyclic appearance of a constellation of symp: tomes prior to menstruation which affect lifestyle or work ‘© Abdominal bloating, anxiety, breast tendemess, depression, and irritability are common symptoms. ‘© The diaguosis does not depend on the specific symptom, but rather on the ability to chart the cyclic nature of the complaint in a predictable fashion. ‘= 40% of reproductive age women report significant problems related to their cycles, but only 1% have such severe PMS that it threatens their work and interpersonal relationships ‘+ The precise cause of PMS is not known. # Fluoxetine (Prozac) and alprazotamn (Xanax) have been shown to reduce symptoms of depression, anger, and anxiety. The mensirual ey3 Abnormal vaginal bleeding CAUSES OF ABNORMAL VAGINAL BLEEDING + ‘eructural (organic) causes Dysfunctional uterine Bieding (OUB) 1 Anovlatery DUB + polystic ovarian syndrome + perimenopausal anovlation {perimerarchal sroniation Endomerral hperpasia 2 Oniatory OUB smideyele Bleeding + short folcular phase long luteal phase 3 Undering myatemic dlaorders thyroid disease Cendcal cancer: cpenbdyaeradte severe organ disease 4 atrogen DUB Glanduiar cei ectrude (One or more polyps oral contraceytives from the conal to portio canbecome ecro% —__Dapo- Provera Norpiant (Geen in pregnancy or imitated, a eroded +2 Johns wortiginseng women on OCP) and cause Deeding Ectropon Foype i FURTHER EVALUATION OF THE UTERUS Performing an endometrial biopey Hysteroscopie evaluation of the uterus Ftd take | Bladder Instrument ports Pipeile to mserved through the cervix 0 the full depth of the endometrial cavity Endometrial polyp | Hycteroscopie held by operative ‘sears forceps [Actual ew Fieton le withdrawn and the sheath jes isd aaa rotated to sample the endometrium ‘hysteroscopy can be both diagnostic and therapeut = procedures that can be performed through the hystercocope Inckide endometrial ablation, polypectomyy (above), submicoeal myomectomy 12 GynecologyDefinitions * Menorehagia refers to prolonged (>7 days) and/or excessive (©80mL) uterine bleeding occurring at regular intervals. © Merrorrhagia refers to variable amounts of uterine bleeding ‘occurring at irregular but frequent intervals + Palymenorchea deseribes an abnormally short interval (21 days) between regular menses * Oligomenorrhea describes an abnormally long interval (35 days) between regular menses. Causes of abnormal bleeding Structural (organic) causes * Pregnancy-related conditions are the most common causes of ‘abnormal vaginal bleeding in reproductive-age women (threatened, incomplete, and missed abortion: ectopic pregnancy: ‘gestational trophoblastic disease). * Urerine lesions commonly produce excessive bleeding by increasing endometrial surface area or distorting endometrial vasculature. * Cervical lesions cause irregular, especially postcoital, bleeding due to erosion or direct trauma, Dysfunctional uterine bleeding Dysfunctional unterine bleeding (DUB) is 2 diagnosis of exclu- sion, referring to abnormal vaginal bleeding. which cannot be explained on the basis of a structural abnormality. The majority ‘of cases represent menstrual irregularities. 1 Anavulatory DUB, Anovulatory cycles are characterized by continuous production of estradiol-178 without corpus Iuteum formation and progesterone release, This unopposed estrogen leads to continuous proliferation of the endometrium which eventually outgrows its blood supply and is sloughed in an iregu- Jar, unpredictable pattern, 2 Ovulatory DUB, Midcycle spotting following the LH surge is "usually physiologic. Polymenorshea is most often due to shorten- ing of the follicular phase of menstruation, Alternatively, the luteal phase may be prolonged by a persistent corpus luteum, 3 Underlying systemic disorders. Abnormal menstrual cycles are ‘occasionally the frst sign of either hyperthyroidism or hypothy- rodism, Blood dyserasias (von Willebrand's disease) commonly present with profuse uterine bleeding during adolescence. Severe ‘organ disease (renal or liver failure) can sometimes result in serious irregular bleeding, 4 Iatrogenic DUB. Oral contraceptives are often associated with irregular bleeding during the first 3 months of use. if doses are missed, oF if the patient is a smoker. Long-acting progesterone-only contraceptives (Depo-Provera, Norplant) frequently cause ieregular bleeding. Some patients may be unknowingly toking herbal medications that have an impact on the endometrium. Diagnosis ‘= The history and physical examination should be focused on determining the site and cause of the bleeding. Patient age is the portant factor in the evaluation. ‘* Ruling out pregnancy-related complications should be the first priority in all reproductive-age women, © A complete list of medications is essenti interference with normal menstruation. + Non-gynecologic physical findings (eg. thyromegaly) may suggest the presence of an underlying systemic disorder. Pelvic ‘examination may reveal an obvious structural abnormality. but frequently additional evaluation is necessary. Abnormal bleeding from the genitourinary (urinary infection) or gastrointestinal systems (hemorrhoids) may be mistaken for gynecologic bleeding. ‘+ Measurement of serum hemoglobin concentration, iron levels, and ferritin levels are objective measures of the quantity and duration of menstrual blood loss. In some cases, other laboratory tests (such as thyroid-stimulating hormone and coagulation profile) may be indicated, ‘© A menstrual calendar may be helpful in accurately determin- the amount, frequency, and duration of the bleeding. ‘© Ovulatory status can be assessed by careful history taking and, if necessary, hasal body temperauure charts, luteal phase serum progesterone levels, ot ovulation prediction kits. ‘= A surgical endomedial biopsy (opposite) can be performed in ‘non-pregnant women to reliably diagnose intrauterine pathology. ‘© Pelvic ulirasound and hysteroscopy may be indicated if the cause of bleeding cannot be identified to rule out their Medical management ‘© The majority of women with abnormal vaginal bleeding can be treated by medical management alone, particularly in the absence of a structural cause # Oral comracepives effectively corsect the vast majority of common menstrual irregularities (anovulatory and ovulatory DUB), However, DUB can occasionally present as an acute hemorrhage requiring short-term, high-dose oral or intravenous premarin (conjugated equine estrogen. ‘© Nonsteroidal anti-inflammatory drugs (such as mefenamic 1) have been shown to reduce menstrual blood loss, particu larly in ovulatory patients. Surgical management ‘= Structural abnormalities frequently require surgical interven tion to achieve alleviation of symptoms, * Dilesation and cureitage (D & C) can be both diagnostic and therapeutic, especially in women with acute vaginal bleeding due to endometrial overgrowth. © Operative hysteroscopy (opposite) is 9 day-surgery procedure that can be used to diagnose and treat abnormal uterine lesions. ‘The uterine cavity is distended with fluid, allowing direct visual: ization of the abnormality and use of hysteroscopic instruments ‘© Hystereciomy is usually reserved for women with structural lesions not amenable to more conservative surgery (multiple large leiomyomas, uterine prolapse). It may also be indicated in ‘women with persistent DUB, but only if medical therapy has failed, Abnormal vaginal bleeding 13Ectopic pregnancy IMPLANTATION SITES AND FREQUENCY RISK FACTORS Tubal (95-972) |nteroiial (commun) (24%) + pelvic Wflammatory deease + prior ectope prewrancy «prior bib aurgery + Cgarette msking + dovehing 1 DES exposure Ovarian (058%) + eavanced maternal age { infereityfoation induction Cental (0%) “Abdominal (0.082) + Inccauterine device DIAGNOSIS MEDICAL THERAPY. Gitera Yor vecelvng methotrexate |Contraindicatlone to wedlal therapy shiatory “enatanccaly ote wou cit ‘Sua tere + earination seuanasr sarc trope Serr weary evsene serial NES Selepecncaps anne ciemusumicy cree encores a ty Necnhon ae hr dene a Snr ene ‘rth Grae hev noes seuldocentesis | ators are ore tr frag care wth upward a Panes hestoconrsnacaion ccesringe || “Sorwnctesne wecioon ‘woh 18 gauge || restive mscare romero ore er tal atede, || Deipures tan Sen ene ‘Nie poor aoa the ceric the seralneedie || Mane aneran sc lero seed adraced | Fertnea ee, | eee Wreo'the posterior | catty ‘ened COD mn : ‘Gesiatooral sac 23.30% vaginal fornia Exnocae nen Eas Netealthergy }——! Surgical therapy] Defi : men totic) Conservative surge (calpingectory) 5 LAPAROSCOPIC LINEAR SALPINGOS TOMY FOR TUBAL ECTOPIC PREGNANCY remacory with \dertication ‘Alvear incoton of tubal preanarey lo made with the fine monopouar \ diathermy nocd ‘ion the ar The men is ‘mesenteric border alone to heal ofthe fallopian tue by secondary imtertion The trophoblastic mace is removed With torcepe and brigaven 14 GynecologyDefinition Fetopic pregnancy is potentially life-threatening condition in ‘which the embryo implants outside the uterine cavity (opposite). Incidence ‘= The incidence of ectopic pregnancy has more than quadrupled in the USA. Currently, 20 cases occur per 1000 pregnancies. '* Ectopic pregnancies account for 10% of prepnancy-related ‘maternal deaths in the USA. Most are attributed to hemorrhage ‘and are potentially preventable. Risk factors + Prior pelvie inflammatory disease (especially that caused by Chlamydia trachomatis) the most important risk factor. Although numerous risk factors are implicated, >S0% of patients with ectopic pregnancy have none Presenting symptoms and signs ‘= Pain remains the most common symptom. Most paticnts also ‘report abnormal vaginal bleeding, usually spotting or slight inter- mittent bleeding. ‘+ Patients with acute rupture present with sharp, tearing. pelvie ‘pain associated with fainting Ten per cent of patients have shoul det tip pain due to diaphragmatic irritation trom intraperitoneal ‘blood. Tachycardia, hypotension, and cervical motion tenderness are associated physica findings. ‘ Historically ewer than 10% of ectopic pregnancies were diag nosed hefore rupture Sensitive blood pregnancy tests and transvaginal ultrasonography have enabled the carlier diagnosis of ectopic pregnancy. As a result, the prognosis for ectopic pregnancy has shifted from ‘grave, life-threatening disease to a more benign condition. Diagnosis © A thorough history and physical examination are essential. “The extent should be dictated by the severity of symptoms at presentation. * Serial quantitative levels of the fbsubunit of human chorionic gonadotropin (PHhCG) are important. In normal early pregnancy, scrum B-ACG levels should double every 48h. © Franvvaginal ultravonography can detect an intrauterine ges- tational sac at a serum frhCG level of 1000-1200 mIU/mL. (45 ‘weeks from LMP), 26000 miU/mL is required to see an intrauter- ine gestational sae by transabdominal sonography. + Culdocentesix (opposite) may be performed in the office or ‘emergency room and can quickly confirm the presence of free blood in the peritoneal cavity: When 10mL. of non-clotting blood is aspirated the testis positive. * Ifthe pregnancy is undesired uterine curetiage can effectively ‘exclude an eetopic pregnancy by demonstrating pathologic evi- dence of products of conception. Management ‘Due 10 earlier diagnosis, the goal of treatment has shifted from preventing mortality to reducing morbidity and preserving fertility. Medical herap, * Methotrexate (MTX) chemotherapy is effective treatment for seleet patients with small, unruptured ectopic preg: nancies, ‘© single intramuscular injection of MTX (SOmg per m’) is administered. followed by serial f-hCG measurements, ‘+ Scrum BCG levels may continue to rise for the first 4 days following MIX injection, An acceptable response is defined as a 218% decrease in serum P+hCG levels from day 4 to day 7. * If an adequate treatment response is achieved, B-hCG levels should be followed weekly until levels are undetectable. ‘Depending on the size of the embryo, most cases will be suc ‘cessfully treated with MTX alone. However, up to 25% require ‘more than one dose. ‘© MIX side-effects (nausea, vomiting) are generally mild. Local- ied, mild abdominal pain is a common complaint following MTX duc to serosal irritation. However, patients should be closely ‘monitored since rupture is a known risk Surgical therapy © Ina patient who is hemodynamically unstable due to rupture ‘ofthe ectopic pregnaney.emergeney surgery (usually laparotomy ‘or without removal of the ruptured fallopian tube) remains the treatment of choice. © Ina hemodynamically stable patient with a ruptured tubal pregnancy, laparoscopy and either removal (salpingectomy) or segmental resection of the tube may be necessary. © Ina hemodynamically stable patient with an unruptured tubal ‘pregnancy, conservative surgery with tubal salvage (laparoscopic ‘and linear salpingotomy) is appropriate (opposite). © If the fallopian tube is not removed, the serum p-hCG level must be followed until detectable. Five to ten per cent of patients will have a persistent eciopie pregnancy which may require further treatment, * Oophorectomy is onl dicated 10 achieve hemostasis: Cervical ectopic pregnaney © A rare but potentially serious form of ecto ddue to the risk of hemorrhage. * Cervical ectopies are usually treated by MTX, ie pregnancy, Interstitial (cornual) ectopic pregnancy ‘* Defined as implantation into the fallopian tube where it passes through the myometrium. © Cornual ectopics usually present Inter in gestation and, if ‘rupture occurs, hemorrhage can be profound. ‘© Cormual resection oF hysterectomy is often required, particu- larly if rapture occurs. © The maternal mortality rate is 2%, Abdominal ectopic pregnancy ‘© Refers to implantation of the embryo in the abdominal cavity. usually deriving its blood supply from the gastrointestinal tract. ‘The diagnosis is often made late and laparotomy with removal cf the fetus is necessary. The umbilical cord is usually clamped and the placenta left ia situ to avoid excessive blood loss. ‘= Abdominal eetopics have with aS-10% maternal mortality and Lp to 95% fetal mortality Ectopic pregnaney 155 Pelvic pain CAUSES OF PELVIC PAN Tubal rupture can lead to hemoperitoneum and shock Bilateral hydrosalpinges following liquification of tubal contents ‘Chubbedt Ectopic pregnancy sees Acute pehic inflammatery disease (PID) ‘Acute appendicitis Perforation may can lead to rupture result ina with abscess formation localized Inthe right: peli abscess Dverticultis Appendicitis Pedicle is rotated on iteelF several ‘times Ovary becomes: ; rlarged, uc hack, et (chocolate cyst) tense ard edematous posterior ‘Ader torsion cude-sec Vterceacraligamont nodularity Endometriosis 16 Gynecology‘© Pelvic pain is subjective perception rather than an objective sensation, making evaluation of the patient difficult, '* Pelvic pain associated with menses is the most common gyne- cologie pain complaint. However. domestic discord, physical or sexual abuse, rape, alcohol ar drug abuse, or ather stresses may all be expressed in the form of pain. Evaluation strategies ‘= The history provides a description of the nature, intensity, and distribution of the pain, However, imprecise localization is typical with intra-abdominal processes ‘© The physical examination includes a comprehensive gyneco- logic examination. Specific attention should be paid to reproduc- ing the pain symptoms. Cultures, serum chemistry and electrolyte evaluations, or ultra- sonography and other imaging studies may be indicated. + Specialized diagnostic studies based on the presumptive diag- nosis may require consultation with other specialists in anesthe- siology. orthopedics, neurology. or gastroenterology. Acute pelvie pain Acute pelvic pain requires aggressive management because of the possibility that a life-threatening condition exists. Gynecologic causes Most general gynecologic causes of acute pelvic pain can be divided into three eategories: infection, rupture, and torsion, ‘© Eciopic pregnancy (opposite and Chapter 4). In all reprodu tive-age women, the first priority in evaluating acute pelvic pai is to rule out the possibility of a ruptured ectopic pregnancy. © Acute pelvic inflammatory disease (PID) (opposite and Chapter 7) is an ascending bacterial infection that usually presents with high fever, acute pelvic pain, and evidence of cervical motion ten- derness in sexually active women. © Rupture of an ovarian eyst. Intraabdominal rupture of follicular cyst, corpus luteum, or endomettioma (opposite) is a ‘common cause of acute pelvie pain. The pain may be so acute and severe as to cause syncope. The condition is usually sel-Limiting ‘with limited intraperitoneal bleeding. ‘© Adnexal torsion (opposite) is seen most commonly in adotes- cent or reproductive-age women. By twisting on its vascular pedicle, any adnexal mass (ovarian dermoid, hydatid of Mor ‘zagni) can cause acute, severe pain by suddenly compromising its ‘blood supply: The pain will frequently wax and wane with asso- ciated nausea and vomiting * Threatened, inevitable, or incomplete abortions axe generally accompanied by midline pelvie pain, usually of a erampy, inter- ‘mittent nature (Chapter 19). = Degencrating fibroids or ovarian tumours way cause localized ‘acute, sharp, or aching pain. ‘Non-gynecologic causes '» Apperulicts (opposite) i the most common acute surgical con- dition of the abdomen, oscuring in all age groups. Classically, the pain is initially diffuse and centred in the umbilical area but. after several hours, localizes fo the right lower quadrant (MeBurney's point). Its often accompanied by low-grade fever, anorexia, and leukocytosis * Diverticulitis. (opposite) occurs mest frequently in older ‘women. It is characterized by left-sided pelvie pain, bloody diar- thea, ever, and leukocytoxix, © Urinary tract disorders (cystitis,pyelonephritis.renal.caeul) ean ‘cause acute or referred suprapubic pain, pressure, and/or dysuria. # Mesenteric lymphadenitis most ofwen follows an upper respira tory infection in young girls The pain is usually more diffuse and less severe than in appendhcitis. Chronic pelvic pain * Chronic pain refers to unrelieved pain that has continued 10 ‘be-a major, disabling condition for at least 6 months. ‘There is often litle correlation between the severity of abo: al discase and the amount of perceived pain, ‘© Depression and sleep disturbance are common associated prychological diagnoses, + Women with chronic pelvic pain are much mor been victims of sexual abuse, One third of women who undergo laparoscopy for chronic pelvic pain will have no identifiable causes * 10-20% of hysterectomies in the USA each year are per formed for chronic pelvie pain. Hysterectomy is highly effective in improving pelvic pain, psychological symptoms, sexual dys- function, and quality of life even if no uterine pathology can be ‘identified, ely to have Gynecologic causes * Dysmenorrhea is the most common cause of ehronie pelvic ‘pain, Ibis dened as eyoic uterine pain occurring before or during ‘menses. Primary dysmenocthea is not associated with pelvic pathology. and is thought to be due to excessive prostaglandin production by the uterus. Secondary dysmenorrhea is usually due to acquired conditions (such as endometriosis) + Endometriosis (opposite and Chapter 11) has a spectrum of ‘pain that ranges from dysmenorrhea to severe, intractable, con uous pain which may be disabling. "The severity of pain need not correlate with the degree of pelvic pathology. * Adenomyosis (Chapter 11) is @ common condition and most iplomatic. An enlarged. boggy uterus that is ly tender on palpation is characteristic. However adeno _myosis remains a pathologic diagnosis, * Fibroids (Chapter 10) are the most frequent (benign) tumours found in the female pelvis. They may cause pain either by putting pressure on adjacent organs or by undergoing degeneration, * Retained ovarian syndrome is characterized. by recurrent adnexal pain after hysterectomy. ** Genital prolapse (Chapter 14) may lead to complaints of heavi ‘ness, pressure, a dropping sensation, or pelvic aching, ‘© Chronic PID is characterized by cominued pelvic pa asa result of hydrosalpinx, tubo-ovarian cyst, or pelvic adhesions. ‘Non-gynecologic causes ‘* Adhesions after infection or surgery may cause chronic pain that is particularty difficult to treat * Gastroimestinal disturbances such a8 infammatory bowel disease (Crohn's disease, ulcerative colitis). iritable howel syn ‘drome, constipation, and fecal impaction can cause pain The pain may be exacerbated around the menses. + Musculoskeletal problems such as faulty posture, muscle strain, (or disk herniation may cause referred pain to the pelvis. Pel pain 176 Infections of the lower genital tract Lesions appear ae multiple, exophytic painiess excreacences ‘around the labia ard perineum. When numerous, they may ave rige to.a confiuent caulfowertie maso Group of vesicles which ‘re fragile and tend to break forming small ulcers «major symptom ace burning pain ana local pruritus VAGINTIS Bacterial vaginosis Condiiasio ‘richomoniasle ‘Thin homogeneous, maladorous Vagina soften Trick white | “Straitery copious (fishy) write grey vagina skacharge | hyperemic and nor-malodorovs. | appearance of reenish-yelow edematous dscharge that | cervn veto ‘echarge wth appoas'cottage | eral petecia frothy appearance cheesetite | hemorrhages Saline net mount a Trchomoade ‘Cue cali with adherent ‘uading yeast, hyphal (robe protozoa Lymphocyces ccocold bacter'a, no fore wth Four Ragliae >OMMer teatocytes, absent iactobacil and central nucleus) Vagina pt >45 (normal 36-42) Vaginal pH<45 (usualy) vaginal p> 45 INFECTIONS OF THE VULVA Genital wares Genital herpes Bartholine gland abscess Tender, red, fuctuant mace occur inthe labia minoral aba majora fold at 5 or 7-dclock “maior symptoms are fever and acute niateral viva pain 18 GynecologyVaginitis ‘Vaginitis is the most common gynecologic problem for which women seek treatment, accounting for >10 million surgery visits each year in the USA, Bacterial vaginosis (opposite) ‘+ Bacterial vaginosis (BV) is not a sexually transmitted disease (STD). tis caused by an overgrowth of several bacterial species, particularly anaerobes # Incidence: the most common cause of va ilubearing age. ‘Symptoms: mild vulvar pruritus and Vaginal discharge © Diognosis: KOH whiff test, pH. >4.5, and saline wetemount. » Treatment: metronidacole (Flagyl) or clindamycin. in women of Candidiasis (opposite) = Candidiasis is not an STD. It is caused by an overgrowth of vaginal fungus, usually Candide albicans, © Incidence: the 2nd most common type of vaginal infection, Symptoms: pruritus and vulvar. itritation. ‘= Diagnosis: KOH wel-mount, and vaginal pH <4. ‘+ Treatment: topical miconazole (Monistal) oF oral uconazole (Diflucan). ‘Trichomoniasis (oppose) ‘© Trichomonas is an STD eaused by the para vaginalis. * Incidence: affects 180 million women worldwide and 3 million ‘women each year in the USA. © Sympioms: a characteristic vaginal discharge. Less commonly. Lysutia, foul odor, or vulvovaginal irritation. © Diagnosis: trichomonads seen on saline wet-mount are pathog- ‘nomonie. Other features include an abundance of leukocytes and 1 vaginal pH 24.5. Organisms may be evident on a PAP smear in asymptomatic women, © Trearment.oral Flagyl Trichomonas Cervicitis Chlamydia © Chlamydia rachomatis is an obligate intracellular bacterial parasite of columnar epithelial cells *# Incidence: the most prevalent STD in the USA. Three to four rillion new cases occur annually. Thirty per cent of infections are associated with gonorthea *# Sympioms: 80% of Women are asymptomatic or have mild, unrecognized symptoms. Most cases are identified through screening or contact tracing. + Diagnosis: rapid DNA probe test or immunosorbent assay. ‘© Treatment: oral azithromycin or doxyeyctine. enzyme-linked Gonorrhea ‘© Neisseria gonorrhoeae is a Gram-negative aerobic diplococcus that grows best in carbon dioxide. © Incidence: >1 million cases oceur each year in the USA. + Symproms: usually asymptomatic. but may include dysuia and « purulent cervical discharge. Ten fo twenty per cent of women develop acute salpingitis with fever and pelvic pain, $% exhibit disseminated gonorthea infection with chills, fever, malaise, asymmetric polyarthralgias, and painful skin lesions. + Diagnosis: postive culture on selective media such as moi fied Thayer-Martin agar. Twenty per cent of patients will have detectable infection at multiple sites (pharynx, rectum). ‘© Treaiment: intramuscular ceftriaxone or oral cefixime. Infections of the vulva Genital warts (opposite) '* Genital warts (condyloma acuminata) are caused by the ‘human papilloma virus (HPV), # Incidence: 750000 new cases annually in the USA. * Symproms: uncomplicated eases are asymptomatic. © Diagnosis; usually clinical inspection is sufficient, but colposcopy and/or biopsy may be required. # Treament, local cytotoxic agents (trichloroacetic acid, podofilox) or ablative therapy (surgery, laser). Genital herpes (opposite) '* Genital herpes isa recurrent STD that is caused by the herpes simplex virus (HSV), predominantly type 2 ‘© Incidence: 500000 new eases cach year in the USA. * Symmproms. First episode primary HSV infection is charact: ferized by systemic symptoms, including malaise and fever. ‘However, genital herpes is recurrent infection with perio of active infection separated by periods of latency. + Diagnosis. Usually clinical inspection is sufficient, but viral isolation by tissue culture is also very reliable. *# Treament. oral aciclovis is caused by the spirochete, Treponema pallidum. + Incidence: 25000 new cases are reported annually in the USA. ‘© Symptoms: primary syphilis usually presents as painless sol ulcer. Secondary syphilis presents as a facial-sparing rash ‘with involvement of the palms and soles The classic skin lesion ‘of late syphilis isthe solitary gumma nodule. © Diagnosis: datk-field examination of secretions from a lesion andlor serologic sereening (rapid plasma reagin (RPR) test), * Treatment. intramuscular benzathine peniciin. Other vulvar infections + Bartholin’s gland abscess (opposite) is treated by surgical inci- sion and placement of a Word catheter. + Pediculosis pubis (scabies) isan STD caused by the erab louse ‘that causes intense vulvar pruritus Lindane (Kwell) isthe treat- ‘ment of choice. Contacts should also be treated. © Molluscum conuagiosum is an asymptomatic, papular STD of the vulvar skin caused by the porvirus Most infections will resolve without treatment, © Necrotizing Jascitis 18 4 rapidly progressive, frequently fatal infection that requires immediate wide surgical debridement and parenteral antibiotics. © Hydradenitis suppurativa is-4 staphylococcal oF streptococcal infection of the vulvar apocrine glands treated by excision. © Rare vulvar STDs include: fymphogranuioma venereum: (caused by Chlamydia machomatis), chanerotd (caused by Haemophilus ducreyi), donovanosis/granuloma inguinale (caused by Calyeamarobacterium granulomas). Infections of the lower genital tract 197 Pelvic inflammatory disease THE CLINICAL SPECTRUM OF ACUTE PELVIC INFLAMMATORY DISEASE (FID) Trick, elonioh micopurvent dbocharge from a fey rea exceral os Infected endometrial glands with premature sloughing end irregular bleeding apron Canes Ascending polynicrobial infection Proerosson — Endomeerta] apap Swollen, erythematous fallopian tubes wth lumen file with pus (Pyoeaipin) TREATMENT OF ACUTE PID 4 Tap OOF papa i root Seip on I Tinea n Cann gin nary hors eer hare oraminleaing dose (2afa flowed by WSaghaln eye howe se hoagie an gon for a at 48 hu at the potas shove scar cel improvement. har hepa! tachorge tr dnyycine XO ma ray te ay shosabe svt to comple day otal Con ns pobre gery retire 220 9 Te Dowyeycre 0 mq erly 2 near ae Rectate 2-9 dae Kegan onan 400 my omy Eten for ays Poe ther naan 420 oat 4 Unity oF retraite 500 mow 2 reno TONG-TERM SEQUELAE OF FID Infertity-due to intraluminal obliteration of ‘the fallopian tubes. pee pain from adnesions and hydrosalpinges Ectople pragnaney-due 2 intraluminal scarring ard Aistortion ofthe fallopian tubes Ruptured TOAS-may develop fllowing incomplete treatment of acute PID 20 Gynecology+ Pelvic inflammatory disease (PID) is the most common com plication of sexually transmitted diseases (STDs) in women, + | million eases of neute PID occur annually in the USA. Definition PID is clinical spectrum of infection (opposite) that may involve one or more of the following structures: the cervix (cer: viciis), the endometrium (endometrits), the fallopian tubes (salpingitis), the ovary (oophorits) the uterine wall (myomett tis), the uterine serosa and broad ligaments (parametrtis), and the pelvie peritoneum (peritonitis). * Acute PID (acute salpingitis) refers to the acute clinical syndrome of ascending infection + Chronic PID refers to the long-term sequelae of such as adhe: sions and hydrosalpinges. Etiology * PID is the result of « polymicrobial infection ascending from the bacterial flora of the vagina and cervix. © Chlamydia trachomatis andlor Neisseria detectable in 250% of women. These pathogens are probably responsible forthe initial invasion of the upper genital tract, with ‘other organisms becoming involved secondarily. + 15% of cases follow a surgical procedure (endometrial biopsy, intrauterine device (IUD) placement) which breaks the cervical ‘mucous barrier and directly transmits vaginal bacteria to the ‘upper genital tact. rorrhoeae are Risk factors PID is a disease of sexually active women. Young age at first crcourse, multiple partners frequency of intercourse, and unmarried status ate all associated with frequency of exposure 10 [STDs and, as such, with PID. + The incidence of acute PID decreases with advancing ape: 75% ‘of patients are <25 years old. + PID isa disease of menstruating women. Its rare during preg. nancy and in premenarchal ar postmenopausal women + There isan increased risk of acute PID in women who have TUD, and a decreased risk among women using either barrier contraception (condom, diaphragm) oral contraceptives. + Previous PID. is risk factor for future episodes: 25% of ‘women will develop future infection. ‘Symptoms and signs * Pain in the lower abdomen and pelvis is the most common symptom, occuring in 390% of patients with acute PID. The pain is usually constant and aggravated by motion + 75% of women have a mucopurulent cervical discharge + 40% have abnormal vaginal bleeding. especially metrorrhagia, + 33% present with a fever 2100.4°F + Nausea and vomiting are usually late symptoms. + 5% of women will present with Fits-Hugh-Curtis syndrome (perihepatic inflammation and adhesions). This condition is char- acterized by pleurtic upper quadrant pain, and is often mistak- ‘nly diagnosed as pneumonia or acute cholecystitis Diagnosis PID is a clinical diagnosis. However, clinical diagnosis is {inexact and up to one third of patients are misdiagnosed, Other conditions that may be mistaken for PLD include acute appen- dicitis, endometriosis, and rupture of an adnexal mass. ‘© Endocervical cultures for chlamydia and gonorrhea should be obtained at presentation, * Ultrasonographic detection of an abscess, purulent fluid on culdocentesis, andor an elevated erythrocyte sediment rate (ESR) may be helpful * The most accurate method of diagnosis of acute PID is direct visualization during laparoscopy. ‘Treatment of acute PID (opposite) ‘ Antibiotic treatment should be started as soon as possible, ‘© 75% of women can be managed as outpatients. If a tuboovarian abscess (TOA) is identified, it should be drained immediately. ‘© Management should include treatment of male partners and education for the prevention of reinfection, Surgical management ‘© Laparotomy is indicated for patients with either a ruptured TOA or a TOA that docs not respond to conservative therapy. ‘= If future fertility is desired, every effort should be made to preserve the reproductive organs. However, bilateral salpingo- ‘cophorectomy with hysterectomy may be required. Long-term sequelae of PID (opposite) + 25% of women who have had acute PID will experience one lor more long-term sequelae. = Inferulty is the most common complication, occurring in 20% of patients. = The risk of ectopic pregnancy is increased 6 10 10-fold in patients with a previous episode of acute PID, © Chronic PID is a common pain syndrome that develops as a result of pelvic adhesions, hydrosalpinges, and other sequelae of inflammation and infection. ‘+ Mortality from PID is rare, but i still high (5-10%) for patients with ruptured TOA (due chiefly to the development of adult respiratory distress syndrome). Rare causes of pelvic inflammatory disease Actinomycosis '* Actinomycosis is a rare cause of upper genital tract infection. ‘© The causative agent is usually Actinomyces israeli, an anaero- bic, Gram-positive. non-acid-fast pleomorphic bacterium. + The diognosis should be suspected if such organisms are iden- tified on cervical Gram stain or if an endometrial biopsy shows ‘sulphur granules’ However definitive diagnosis requires a posi- tive culture. ‘= Treatment: high-dose parenteral penicillin plus oral doxyey- cline for 6 weeks Pelvic tuberculosis = Pelvic tuberculosis (TB) is rare in the USA, but is 2 common cause of chronic PID and infertility in the third world. “The causative agent is usually Mycobacterium tubereuloss ‘= Definitive diagnosis requires histological evidence of granulo- ‘mas, giant cells and cascous necrosis. ‘© Treatment: multiple antituberculosis drugs for 18-24 months, Pelvic inflammatory disease 2