Medstar Obstetrics and Gynecology 2nd Edition PDF
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Jimma University
2023
Graduating Class of Jimma University
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This is a clinical guide and synopsis for Obstetrics and Gynecology for the graduating class of Jimma University 2022/23. It covers topics like antenatal care, fetal well-being assessment, and hypertensive disorders of pregnancy. The guide is organized in a case-oriented approach.
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CLINICAL GUIDE AND SYNOPSIS Prepared By FOR The Graduating Class of Jimma University REVISION ONLY 2015 e.c (2022/23) MEDSTAR CLINICAL GUIDE AND SYNOPSIS OBSTETRICS AND GYNECOLO...
CLINICAL GUIDE AND SYNOPSIS Prepared By FOR The Graduating Class of Jimma University REVISION ONLY 2015 e.c (2022/23) MEDSTAR CLINICAL GUIDE AND SYNOPSIS OBSTETRICS AND GYNECOLOGY SECOND EDITION DEC, 2022 Prepared by Graduating Class of Jimma University 2015 EC (2022/23) Medstar Obstetrics and Gynecology Second Edition I Preface The second edition of MEDSATR CLINICAL GUIDE AND SYNOPSIS TO OBSTETRICS AND GYNECOLOGY (OBGYN) is one of the three similar works, which include similar sister documents for Internal medicine and Pediatrics. The second edition is prepared based on the positive feedbacks & the constructive criticism we received from the previous one. In this edition we have tried to include more topics and updates. The guide is mainly prepared by combining our ward experience and the detailed science on textbooks for the major cases in obstetrics and gynecology. The approach we used is case oriented. The management plans for the most cases is mainly taken from the FMOH Obstetrics management protocol and Jimma University OBGYN Management Guideline. For history and physical examination in OBGYN we strongly recommend you to read, Introduction to Obstetrics and Gynecology diagnosis, by Dr. Asheber Gaym. You should also check the simplified format for history taking and physical examination prepared by Jimma Medical Center OBGYN Department. In conclusion, we would like to say, we have tried to make this guide as readable as possible and we hope it will come in handy for revision in a short period of time. We have prepared an Email address and Telegram bot link so that we could get your feedback on the book and come up with a better second edition in upcoming years. Email address: [email protected] The Contributors Prepared by Graduating Class of Jimma University 2015 EC (2022/23). Medstar Obstetrics and Gynecology Second Edition II Acknowledgment We would like to express our sincere gratitude to the medical students who have sacrificed their time in relentlessly committing to this book. Special thanks are due to Dr. Rajif Shawl (Medstar Coordinator and Medstar Internal Medicine organizer) for his initiative and encouragement to prepare this document. Prepared by Graduating Class of Jimma University 2015 EC (2022/23). Medstar Obstetrics and Gynecology Second Edition III Contributors Dr. Balkewkal Kebede (MI) Dr. Daniel Delessa (MI) Dr. Abubeker Nuredin (MI) Dr. Amanuel Tefera (MI) Dr. Bulcha Lemma (MI) Dr. Abdulhafiz Hussein (MI) Dr. Birhanu Olani (MI) Dr. Bethel Ayele (MI) Dr. Abraham Gebeyehu (MI) Dr. Bemnet G/Micheal (MI) Coordinator: Dr. Balkewkal Kebede (MI) Cover page by: Dr. Nahom Asnake (Nax, MI) Prepared by Graduating Class of Jimma University 2015 EC (2022/23). Medstar Obstetrics and Gynecology Second Edition IV Medstar OBGYN Team Prepared by Graduating Class of Jimma University 2015 EC (2022/23). Medstar Obstetrics and Gynecology Second Edition V Contents Preface......................................................................................................................................................... I Acknowledgment...................................................................................................................................... II Contributors............................................................................................................................................. III SECTION ONE: OBSTETRICS.................................................................................................... 15 Chapter 1..................................................................................................................................................... 1 ANTENATAL CARE (ANC)....................................................................................................................... 1 Definition, Classification and Objectives of ANC........................................................................ 1 First ANC contact.................................................................................................................................. 4 Diagnosis of pregnancy.................................................................................................................. 4 Gestational age determination..................................................................................................... 6 Detail Hx, P/E and Baseline IXs.................................................................................................... 8 Subsequent ANC contacts................................................................................................................ 10 Functions of Obstetric Ultrasound................................................................................................ 11 First trimester U/S......................................................................................................................... 11 Second and Third Trimester U/S................................................................................................ 12 Anemia in pregnancy........................................................................................................................ 13 HIV in pregnancy............................................................................................................................... 16 Syphilis in pregnancy........................................................................................................................ 16 Viral hepatitis in pregnancy............................................................................................................ 20 UTI in pregnancy................................................................................................................................ 21 Acute urethritis/acute urethral syndrome.............................................................................. 21 Asymptomatic Bacteriuria and Acute Cystitis........................................................................ 22 Acute Pyelonephritis..................................................................................................................... 24 Rh alloimmunization........................................................................................................................ 26 Chapter 2.................................................................................................................................................. 27 Antenatal Assessment of Fetal Well Being...................................................................................... 27 Introduction........................................................................................................................................ 27 Modalities of antepartum testing.................................................................................................. 30 Chapter 3.................................................................................................................................................. 40 ASSESSMENT OF FETAL PULMONARY MATURATION................................................................ 40 Tests of Fetal Pulmonary Maturity................................................................................................ 41 Prepared by Graduating Class of Jimma University 2015 EC (2022/23). Medstar Obstetrics and Gynecology Second Edition VI Antenatal Corticosteroid Therapy (ACS)...................................................................................... 45 Chapter 4.................................................................................................................................................. 50 HYPERTENSIVE DISORDERS OF PREGNANCY (HDP)................................................................. 50 Definition and Classifications........................................................................................................ 50 Gestational HTN (GH)....................................................................................................................... 53 Preeclampsia (PE).............................................................................................................................. 54 Eclampsia............................................................................................................................................. 67 Chronic HTN and Superimposed PE............................................................................................. 70 Superimposed PE................................................................................................................................ 71 Management of PE-E syndrome..................................................................................................... 71 Management of eclampsia............................................................................................................... 78 Subsequent risks of women who developed HDP..................................................................... 79 SAMPLE HISTORY.............................................................................................................................. 80 Chapter 5.................................................................................................................................................. 85 ANTEPARTUM HEMORRHAGE (APH)............................................................................................. 85 Causes of Third-Trimester bleeding.............................................................................................. 86 Placental Abruption.......................................................................................................................... 87 Placenta Previa................................................................................................................................... 93 Morbidly adherent placentas.......................................................................................................... 97 Vasa Previa......................................................................................................................................... 100 SAMPLE HISTORY............................................................................................................................ 102 Chapter 6................................................................................................................................................ 105 PROM & PRETERM LABOR............................................................................................................... 105 PRETERM LABOR/BIRTH.............................................................................................................. 105 PREMATURE/PRELABOR RUPTURE OF MEMBRANE (PROM)........................................... 111 Sample history.................................................................................................................................. 118 Chapter 7................................................................................................................................................ 121 MALPRESENTATION........................................................................................................................... 121 Introduction...................................................................................................................................... 121 Incidence and Etiologies/Risk factors........................................................................................ 123 Breech presentation........................................................................................................................ 124 Face presentation............................................................................................................................. 135 Prepared by Graduating Class of Jimma University 2015 EC (2022/23). Medstar Obstetrics and Gynecology Second Edition VII Brow presentation........................................................................................................................... 138 Compound presentation.............................................................................................................. 140 Shoulder presentation (Transverse lie)...................................................................................... 142 Chapter 8................................................................................................................................................ 146 MULTIFETAL GESTATION................................................................................................................. 146 Twin pregnancy................................................................................................................................ 147 Monozygotic twins............................................................................................................................ 147 Dizygotic twins.................................................................................................................................. 151 Diagnosis of MG............................................................................................................................... 153 Complications of MG....................................................................................................................... 154 Management of MG pregnancies................................................................................................. 160 Chapter 9................................................................................................................................................ 165 Red Cell Alloimmunization (Rh Alloimmunization).................................................................. 165 Introduction...................................................................................................................................... 165 Rh (CDE) Blood Group Incompatibility..................................................................................... 168 Management of Pregnancy in Rh Negative Women................................................................ 171 Management of ICT Negative Pregnancy – Prevention of Sensitization............................ 172 Antepartum Prophylaxis for Pregnancy Complications with FMH................................................... 174 Postpartum prophylaxis.................................................................................................................... 175 Management of ICT Positive Pregnancy - the Alloimmunized pregnancy........................ 179 Outcomes........................................................................................................................................... 184 Hemolytic Disease of the Fetus and Newborn (HDFN)..................................................................... 185 Chapter 10............................................................................................................................................... 187 GESTATIONAL DIABETES MELLITUS (GDM).................................... Error! Bookmark not defined. Types of DM....................................................................................................................................... 187 Pathophysiology of GDM............................................................................................................... 189 Screening and Diagnosis................................................................................................................ 190 Complications of diabetes during pregnancy........................................................................... 191 Congenital Malformations................................................................................................................ 192 Fetal Macrosomia............................................................................................................................. 193 Neonatal Hypoglycemia.................................................................................................................... 194 Respiratory Distress Syndrome......................................................................................................... 194 Prepared by Graduating Class of Jimma University 2015 EC (2022/23). Medstar Obstetrics and Gynecology Second Edition VIII Management of DM during pregnancy....................................................................................... 195 Management of the patient with type 1 or type 2 DM.................................................................... 195 Management of the woman with GDM............................................................................................ 202 Long-Term Effects of Glucose Intolerance on Mother and Fetus..................................................... 204 Pre-pregnancy counseling of women with preexisting diabetes mellitus........................ 205 Chapter 11............................................................................................................................................... 206 Intrauterine Growth Restriction/Retardation............................................................................. 206 Introduction...................................................................................................................................... 206 Etiologies of IUGR............................................................................................................................ 210 Diagnosis of FGR.............................................................................................................................. 212 Management...................................................................................................................................... 217 Chapter 12............................................................................................................................................... 220 Amniotic fluid disorders.................................................................................................................... 220 Introduction...................................................................................................................................... 220 Assessment of AFV........................................................................................................................... 221 Oligohydramnios............................................................................................................................. 222 Polyhydramnios/hydramnios....................................................................................................... 225 Chapter 13............................................................................................................................................... 229 POSTPARTUM HEMORRHAGE (PPH)............................................................................................ 229 Introduction...................................................................................................................................... 229 Classification..................................................................................................................................... 230 Etiology............................................................................................................................................. 230 Late PPH............................................................................................................................................ 246 Chapter 14............................................................................................................................................... 251 Intra-amniotic Infection (Chorioamnionitis)............................................................................... 251 Introduction...................................................................................................................................... 251 Pathogenesis..................................................................................................................................... 251 Epidemiology.................................................................................................................................... 252 Clinical presentation....................................................................................................................... 253 Diagnosis............................................................................................................................................ 254 Management...................................................................................................................................... 255 Complications................................................................................................................................... 258 Prepared by Graduating Class of Jimma University 2015 EC (2022/23). Medstar Obstetrics and Gynecology Second Edition IX Prevention......................................................................................................................................... 259 Chapter 15............................................................................................................................................... 260 Puerperal Fever.................................................................................................................................... 260 Definitions......................................................................................................................................... 260 Differential Diagnosis for Puerperal fever................................................................................ 261 Postpartum endomyometritis........................................................................................................... 261 SECTION TWO: GYNECOLOGY..................................................................................................... 272 Chapter 16............................................................................................................................................... 273 ABDOMINOPELVIC MASS (APM).................................................................................................... 273 Approach............................................................................................................................................ 273 Differential diagnosis of APM....................................................................................................... 278 Chapter 17............................................................................................................................................... 287 Approach to Abnormal Uterine Bleeding...................................................................................... 287 Definitions......................................................................................................................................... 287 Incidence and Etiology................................................................................................................... 290 Endometrial cancer........................................................................................................................... 298 Patient Evaluation........................................................................................................................... 301 Chapter 18............................................................................................................................................... 304 LEIOMYOMAS....................................................................................................................................... 304 Factors associated with leiomyoma............................................................................................ 305 Pathophysiology............................................................................................................................... 306 Classification..................................................................................................................................... 307 Secondary changes in myoma....................................................................................................... 308 Clinical features................................................................................................................................ 310 Differential diagnosis..................................................................................................................... 313 Complications................................................................................................................................... 313 Myomas and Pregnancy.................................................................................................................. 313 Management...................................................................................................................................... 314 Sample History................................................................................................................................. 323 Chapter 19............................................................................................................................................... 327 OVARIAN TUMORS............................................................................................................................. 327 Epidemiology and Risk factors..................................................................................................... 327 Prepared by Graduating Class of Jimma University 2015 EC (2022/23). Medstar Obstetrics and Gynecology Second Edition X Prevention of Ovarian Cancer...................................................................................................... 330 Classification of Ovarian Tumors................................................................................................ 333 Benign Ovarian Masses..................................................................................................................... 334 Borderline Ovarian Masses............................................................................................................... 336 Malignant Ovarian Masses................................................................................................................ 337 Epithelial Ovarian Cancer.................................................................................................................. 337 Differentiating between malignant and Benign ovarian masses...................................................... 342 Malignant Ovarian Germ Cell Tumors.............................................................................................. 349 Ovarian Sex Cord-Stromal Tumors (SCST)......................................................................................... 352 Ovarian cancer during pregnancy............................................................................................... 355 Sample history.................................................................................................................................. 357 Chapter 20.............................................................................................................................................. 359 CERVICAL NEOPLASIA....................................................................................................................... 359 Cervical Intraepithelial Neoplasm (CIN)................................................................................... 359 Pathogenesis and Risk factors........................................................................................................... 360 CIN and Human papilloma Virus (HPV)............................................................................................. 362 Cervical Cancer Prevention and Screening............................................................................... 365 Cervical cancer.................................................................................................................................. 373 Sample history.................................................................................................................................. 381 Chapter 21............................................................................................................................................... 383 GESTATIONAL TROPHOBLASTIC DISEASE.................................................................................. 383 Definitions......................................................................................................................................... 383 Classification..................................................................................................................................... 383 Epidemiology and Risk factors..................................................................................................... 384 Pathogenesis..................................................................................................................................... 385 Clinical features................................................................................................................................ 387 Complications................................................................................................................................... 391 Treatment of Benign GTD.............................................................................................................. 392 GESTATIONAL TROPHOBLASTIC NEOPLASIA........................................................................ 394 SAMPLE HISTORY............................................................................................................................ 404 Chapter 22.............................................................................................................................................. 407 Pelvic Pain.............................................................................................................................................. 407 Prepared by Graduating Class of Jimma University 2015 EC (2022/23). Medstar Obstetrics and Gynecology Second Edition XI Classification..................................................................................................................................... 407 Acute pelvic pain.............................................................................................................................. 408 DDx for Acute pelvic pain.................................................................................................................. 408 Cyclic pelvic pain.............................................................................................................................. 416 Chronic pelvic pain.......................................................................................................................... 417 DDx Chronic Pelvic Pain.................................................................................................................... 418 Endometriosis................................................................................................................................... 419 Adhesion........................................................................................................................................... 423 Approach to Pelvic/lower abdominal pain................................................................................ 424 Chapter 23............................................................................................................................................... 429 ABORTION............................................................................................................................................. 429 Definition and Terminology......................................................................................................... 429 Spontaneous first trimester abortion......................................................................................... 430 Etiologies and Risk Factors................................................................................................................ 431 Clinical classification of spontaneous abortion................................................................................. 433 Spontaneous midtrimester abortion.......................................................................................... 436 Induced abortion............................................................................................................................. 437 Complication of abortion............................................................................................................... 438 Approach............................................................................................................................................ 438 Management...................................................................................................................................... 440 Spontaneous abortion...................................................................................................................... 440 Induced abortion............................................................................................................................... 441 Components of Post abortion care (PAC)......................................................................................... 442 Chapter 24.............................................................................................................................................. 443 Ectopic pregnancy................................................................................................................................ 443 Definition and terminology.......................................................................................................... 443 Risk factors........................................................................................................................................ 444 Pathophysiology............................................................................................................................... 445 Clinical manifestation.................................................................................................................... 446 Diagnosis............................................................................................................................................ 447 Management...................................................................................................................................... 449 Chapter 25............................................................................................................................................... 453 Prepared by Graduating Class of Jimma University 2015 EC (2022/23). Medstar Obstetrics and Gynecology Second Edition XII PELVIC INFLAMMATORY DISEASE................................................................................................. 453 Etiology............................................................................................................................................... 453 Pathogenesis..................................................................................................................................... 454 Risk factors for PID......................................................................................................................... 456 Clinical manifestation.................................................................................................................... 457 DIAGNOSIS........................................................................................................................................ 458 Complication..................................................................................................................................... 461 Treatment.......................................................................................................................................... 462 Chapter 26.............................................................................................................................................. 466 HYPEREMESIS GRAVIDARUM (HEG)............................................................................................. 466 Definition and Incidence............................................................................................................... 466 Pathogenesis..................................................................................................................................... 466 Risk factors........................................................................................................................................ 468 Approach............................................................................................................................................ 469 Management...................................................................................................................................... 473 Chapter 27.............................................................................................................................................. 477 PELVIC ORGAN PROLAPSE............................................................................................................... 477 Definition and Epidemiology........................................................................................................ 477 Pathophysiology............................................................................................................................... 477 Description and classification...................................................................................................... 481 POP Quantification system............................................................................................................... 482 Baden-Walker Halfway system......................................................................................................... 484 Clinical manifestations of POP.................................................................................................... 485 Management principle................................................................................................................... 487 SAMPLE HISTORY............................................................................................................................ 491 Chapter 28.............................................................................................................................................. 494 INFERTILITY.......................................................................................................................................... 494 Definitions and Classification...................................................................................................... 494 Etiologies............................................................................................................................................ 495 Approach to Infertility.................................................................................................................... 495 Evaluation for Infertility................................................................................................................ 500 Evaluation of Female Infertility......................................................................................................... 500 Prepared by Graduating Class of Jimma University 2015 EC (2022/23). Medstar Obstetrics and Gynecology Second Edition XIII Evaluation of male infertility............................................................................................................. 510 Treatment.......................................................................................................................................... 512 Chapter 29.............................................................................................................................................. 514 AMENORRHEA..................................................................................................................................... 514 Primary amenorrhea....................................................................................................................... 514 Etiologies........................................................................................................................................... 515 Evaluation of primary amenorrhea................................................................................................... 521 Management..................................................................................................................................... 528 Secondary amenorrhea................................................................................................................... 530 Evaluation of secondary amenorrhea............................................................................................... 536 Management..................................................................................................................................... 539 Chapter 30.............................................................................................................................................. 541 GENITOURINARY FISTULA (GUF)................................................................................................... 541 Physiology of Micturation............................................................................................................. 541 Urinary Incontinence...................................................................................................................... 542 Genitourinary fistula....................................................................................................................... 542 Incidence........................................................................................................................................... 542 Classification..................................................................................................................................... 543 Etiology and Risk factor..................................................................................................................... 545 Pathophysiology................................................................................................................................ 547 Clinical manifestation........................................................................................................................ 548 Diagnosis........................................................................................................................................... 548 Complications.................................................................................................................................... 549 Management..................................................................................................................................... 550 Prevention......................................................................................................................................... 551 Sample history.................................................................................................................................. 552 References.............................................................................................................................................. 553 Prepared by Graduating Class of Jimma University 2015 EC (2022/23). This page is intentionally left blank Prepared by Graduating Class of Jimma University 2015 EC (2022/23). SECTION ONE: OBSTETRICS Prepared by Graduating Class of Jimma University 2015 EC (2022/23). Medstar Obstetrics and Gynecology Second Edition 1 Chapter 1 ANTENATAL CARE (ANC) Prepared by Dr. Balkewkal Kebede (MI) Definition, Classification and Objectives of ANC Antenatal care (ANC) is defined as the complex of interventions that a pregnant woman and adolescent girl receives from skilled health care professionals in order to ensure the best health conditions for both mother and baby during pregnancy. Timely and appropriate ANC: - o reduces complications from pregnancy and childbirth o reduces stillbirth and perinatal death Historically the practice of comprehensive and organized delivery of ANC passed through three phases Traditional ANC model Focused ANC model ANC for a positive pregnancy experience, (New WHO 2016 ANC model) o The new model uses the term contact between a pregnant woman and a health care provider. o Objectives (what it means to have positive pregnancy experience) A health pregnancy for mother and baby (including preventing or treating risks, illness and death Physical and sociocultural normality during pregnancy Effective transition to positive labour and birth Positive motherhood (including maternal self-esteem, competence and autonomy) ANC contacts Generally prenatal care can be classified in to: - Basic Care and Specialized Care WHO (2016) recommends at least eight ANC contacts as a basic prenatal care for all pregnant women. Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 2 Specialized care is given to pregnant ladies with risk factors associated with adverse pregnancy outcomes. The specific risk factors are listed in the FMOH integrated pregnancy, labor, delivery, newborn and postnatal care card. Basic prenatal care schedule 1st contact in the 1st TM, up to 12wks of gestation 2nd and 3rd contacts in the 2nd TM, @20th and 26thwks of gestation 4th - 8th contacts in the 3rd TM, @30th, 34th, 36th, 38th & 40thwks of gestation What are the general aims/objectives/components of ANC? Early detection and management of preexisting disease DM, HTN, Cardiac, thyroid Early detection and management of pregnancy complications Early Late o Ectopic o HDP pregnancy o APH o Molar o GDM pregnancy o PTL o Abortion o PPROM/PROM o HEG... o Malpresentation o Anemia… Health promotion and disease prevention o What do you promote? o Good Nutrition and rest o Abstinence from Harmful substance (tobacco, alcohol, traditional remedies) o Hygiene and infection prevention practice o Breast feeding o Family planning o What do you prevent? o Anemia=> o Fe and folate supplementation, with 30 mg to 60 mg of elemental iron and 400μg (0.4 mg) of folic acid o What is the elemental iron in different preparations of iron? Fe supplementation is also recommended to prevent puerperal sepsis, LBWt and preterm labor (Ayder’s) Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 3 Intermittent Fe (120 mg elemental iron) and folic acid(1280μg) weekly is recommended if daily iron is not acceptable due to side effects (Ayder’s) o Deworming=>using single-dose albendazole (400mg) or mebendazole (500 mg) is recommended after the first trimester in endemic areas (areas with greater than 20% prevalence of infection with any soil- transmitted helminths) o Neonatal tetanus=> Td-Immunization, A total of five doses needs to be administered, 1st dose at 1st visit/contact, 2nd dose 1 month from 1st dose, 3rd dose 6month from 2nd dose, 4th dose after 1yr and last dose after 1yr from 4th. The level and duration of protection increases with each dose. TT Level of protection Duration of protection TT1 Nil None TT2 80% 3rys TT3 95% 5yrs TT4 99% 10yrs TT5 99% 30yrs NB. Most mothers take only the 1 two, and won’t return for the st remaining doses after delivery o HIV(PMTCT)=> start/continue ART Option “B plus” = start treatment right after dx, irrespective of the CD4 o Malaria=> ITNs o HDFN (HDN/erythroblastosis fetalis) => Anti-D Ig in non-sensitized Rh- negative women at 28th and 34th wks of gestation o Viral hepatitis (fulminant & chronic hepatitis in the neonate) => see below o Calcium deficiency=>1.5–2.0 g oral elemental calcium starting from 14 weeks of gestation o Preeclampsia=> low dose Aspirin(50-150mg) is given for women, who is considered to have high risk for PE, like those with Hx of PE with adverse outcome Chronic HTN MG Comorbidities like DM (type 1 or 2), renal disease Autoimmune disease (SLE, Antiphospholipid antibody syndrome) Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 4 Should be initiated between 12 and 28wks of gestation (optimally before 16wks), and continuing till delivery Birth preparedness and complication readiness Advise on the need to prepare place of delivery and a skilled attendant, money, transportation, social/family support… Readiness for any complication during or after delivery, especially for high- risk pregnancies First ANC contact Objectives: Confirmation of pregnancy Gestational Age (GA) determination Detail Hx, P/E and Baseline IXs Diagnosis of pregnancy Not all amenorrhea and/or protuberant abdomen is pregnancy/a baby. You need to widen your approach when evaluating a lady presenting with amenorrhea and/protuberant abdomen The manifestations of pregnancy can be classified into three groups: -Presumptive, Probable and Positive Presumptive manifestations Amenorrhea => the abrupt cessation of menses in a healthy reproductive-aged female with predictable cycles is highly suggestive of pregnancy Nausea and vomiting (morning sickness) o Occur in 50% of pregnancies), starting as early as 2wks of gestation and usually resolves at 13th-16thwks of gestation o HEG- is a severe form of nausea and vomiting characterized by dehydration, weight loss (up to 5%) and ketonuria. (See chapter) o Advice the women to have frequent small meals, dry diet, and provide emotional support Breast changes o Mastodynia o Breast engorgement o Colostrum secretion=> can occur as early as 16thwks of G o Development of secondary breast tissue along the nipple line Elevated basal body temperature=>progesterone produces a 0.5°F increase in the basal body temperature, which persists after the missed menses. Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 5 Quickening => initial fetal movement perception by the mother, occurs at around 16th-18thwks of gestation in multiparous and 18th-20thwks of gestation in primiparous women Skin changes o Chloasma/mask of pregnancy=> darkening of the forehead, bridge of the nose and cheeks Occur after 16thwks of gestation and is linked to genetic predisposition Exacerbated by sunlight o Linea nigra & nipple darkening+> MSH associated o Stria marks, on breast, abdomen Appear late in pregnancy and is associated with collagen separation o Spider telangiectasia and palmar erythema=> due to elevated estrogen Bladder irritability, frequency, nocturia, UTI Probable Manifestations Pelvic organ changes Chadwick’s sign=> bluish discoloration of the vagina and cervix Due to congestion of the pelvic vasculature Hegar’s sign=> widening and softening of the body or isthmus of the uterus, occur @6th-8thwks of gestation Leukorrhea Relaxation of pelvic ligaments Abdominal enlargement Uterine contraction (Braxton Hick’s contraction,) Positive signs of pregnancy Fetal heart tone=>are detectable by handheld Doppler (after 10 weeks’ gestation) or by fetoscope (after 18–20 weeks’ gestation). Uterine Size/Fetal Palpation=>the fetus can be palpated through the maternal abdominal wall (after 22 weeks), and the position can be determined by Leopold’s maneuvers. Imaging Studies Sonography (ultrasound) is one of the most useful technical aids in diagnosing and monitoring pregnancy. Cardiac activity is discernible at 5–6 weeks via transvaginal sonogram, limb buds at 7–8 weeks, and finger and limb movements at 9–10 weeks. At the end of the embryonic period (10 weeks by LNMP), the embryo has a human appearance. Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 6 The GA can be determined by the crown rump length (CRL) between 6- and 13-weeks’ gestation, with a margin of error of approximately 8% or 3–5 days. See more about function of obstetric ultrasound below. Pregnancy Tests Sensitive, early pregnancy tests measure changes in the level of human chorionic gonadotropin (hCG) The β submit of hCG is produced by the syncytiotrophoblast 8 days after fertilization and may be detected in the maternal serum 8–11 days after conception or as early as 21–22 days(3wks) after the LNMP. β-hCG levels peak at 10–12 weeks’ gestation and decrease afterward Generally, serum and urine levels return to normal ( if u hear the fetal heart beat with fetoscope, the GA must be at least…? Serial fundal height=> is generally not recommended o Between 18 & 34-weeks’ gestation, the uterus size or fundal height measured in centimeters from the pubic symphysis to the upper edge of the uterine corpus, correlates well with the GA in weeks Quickening, (never seen it used, personally) Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 8 NB. Only Early U/s and Reliable LNMP is routinely used for GA determination in our setup, Detail Hx, P/E and Baseline IXs So, you have confirmed it is a pregnancy and determined the GA with the most accurate available method. Next step on the 1st ANC contact is to: - Take detail current & past obstetric and general medical hx, o which will help you to classify which type of care you are going to provide to the women, Let’s see some important points to focus on the hx o Age=> age extremes are common risk factors for many obstetric complications Young age (adolescent pregnancy) Preeclampsia-eclampsia IUGR, low birthweight (LBWt) Maternal malnutrition Labor abnormalities, like OL/CPD Older age Abortion MG, GDM, Chromosomal abnormalities APH(PA&PP), PPH, Uterine rupture Malpresentation PTL, PROM o Mode of conception (spontaneous Vs ART) Conception using ART is a risk factor for MG, PTL/preterm delivery, perinatal mortality, congenital anomalies, LBWt. o Any exposure to teratogens, harmful substance o Danger signs, the one thing your ANC Hx (any Hx of a pregnant lady) shouldn’t miss is assessment of danger signs. Like Vaginal bleeding, HA, ABM, Blurring of vision Leakage of liquor (may be confused with vaginal discharge syndrome, therefore do sterile speculum examination, abdominal pain (lower as well as epigastric) decreased fetal movement, vertigo, tinnitus, palpitation high grade fever Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 9 o Past obstetrics Hx, Almost all pregnancy associated complications in a previous px are risk factors for subsequent pregnancy, with increasing percentage nonetheless. When do we say bad obstetric hx (BOH)? Ans. When a woman has hx of o recurrent abortion (2 abortions for age 35,) o stillbirth, o early neonatal death (within 1wk postpartum) For a woman with hx of previous infant with genetic disorder or/& congenital anomalies, cytogenic testing is recommended prior to conception Rh-alloimmunization (maternal BG) Interpregnancy interval (interval >7yrs is considered too long and is a risk factor for similar complications associated with young age, and interval 25 mm, the absence of an embryo with a heartbeat more than 2 weeks after a scan showed a gestational sac without a yolk sac, and the absence of an embryo with a heartbeat more than 11 days after a gestational sac with a yolk sac was seen o If there are borderline findings and uterine evacuation is being considered, it is prudent to repeat the ultrasound in 7 to 10 days to be absolutely certain that a viable pregnancy is not interrupted. GA determination Identification of chromosomal abnormalities o First-trimester ultrasound findings predictive of a chromosome abnormality include: A thick nuchal translucency, absent nasal bone, Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 12 abnormally fast or slow fetal heart rate, and some structural malformations Second and Third Trimester U/S Components/functions of 2nd and 3rd TM U/S Fetal cardiac activity (present or absent, normal or abnormal) and fetal wellbeing assessment (BPP, in 3rd TM) Fetal growth assessment, estimation of fetal weight (Dx of IUGR) o Repeated ultrasound exams for growth should be performed at least 2 to 4 weeks apart Number of fetuses (Dx of MG) (if multiples, document chorionicity, amnionicity, comparison of fetal sizes, estimation of amniotic fluid normality in each sac, and fetal genitalia) Qualitative or semiquantitative estimate of amniotic fluid volume (Dx of oligohydramnios or polyhydramnios) Placental location, especially its relationship to the internal Os, and placental cord insertion site (Dx of placenta previa and vasa previa) o The diagnosis of vasa previa is critical because the recognition of this finding at the time of a screening ultrasound greatly affects the chance of fetal survival; the fetal mortality rate is high when vasa previa is not diagnosed before labor. Evaluation of the uterus that includes fibroids (Dx of tumor previa), adnexal structures, and the cervix (short cervix, as measured with transvaginal ultrasound, is associated with an increased risk of preterm birth) Anatomic survey to include: o Head and neck Dx of NTD and associated cranial abnormalities Dx of cleft lip and cleft palate approximately two thirds of those with cleft lip also have cleft palate, Nuchal skin fold may be helpful for aneuploidy risk o Chest Four-chamber view of the heart & Outflow tracts (if possible) o Abdomen Stomach (presence, size, and situs, dx of duodenal atresia) Kidneys & Bladder Umbilical cord insertion into the abdomen Number of umbilical cord vessels Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 13 o Spine o Extremities (presence or absence of legs and arms) Gender determination Presentation Anemia in pregnancy Most clinicians diagnose anemia when the hemoglobin concentration is less than 11 g/dL or the hematocrit is less than 32%. Using these criteria, 50% of pregnant women are anemic. Physiologic anemia of pregnancy Occurs because of disproportionate expansion of the plasma volume and the RBC mass During a singleton pregnancy, maternal plasma volume gradually expands by approximately 50% (1000 mL). The total RBC mass also increases but only by approximately 300 mg (25%), and this starts later in pregnancy By 6th weeks postpartum, in the absence of excessive blood loss during the puerperium, hemoglobin and hematocrit levels have returned to normal if the mother has adequate iron stores Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 14 Iron deficiency anemia (IDA) Approximately 75% of anemia that occurs during pregnancy is secondary to iron deficiency There is ~2.3g of total body iron in women (~65% of this is in RBCs) An additional 1g(6-7mg/day) iron is needed to support the RBC mass increment(450mg), fetus & placenta(360mg) and the loss during delivery(190mg) Predisposing factors for IDA o Poor dietary intake o Short interpregnancy interval (Iron deficient erythropoiesis=>IDA (defined by the identification of microcytic hypochromic RBCs) o The first pathologic change to occur in iron deficiency anemia is the depletion of bone marrow, liver, and spleen iron stores. This may take a few weeks to a few months depending on the level of the woman’s iron stores o Over a period of a few weeks, the serum iron level falls, as does the percentage saturation of transferrin. The total iron-binding capacity (TIBC) rises simultaneously with the fall of iron, because this is a reflection of unbound transferrin. o A falling hemoglobin and hematocrit follow within 2 weeks. Microcytic hypochromic RBCs are released into the circulation. NB. If iron deficiency is combined with folate/Vit B12 deficiency, normocytic (normal MCV) normochromic RBCs are observed in peripheral morphology Lab parameters in IDA o Low MCV, MCH, MCHC, and increased RDW on CBC o Serum iron the urine usually has WBCs, but bacteria may not be consistently present. Urine cultures may have low colony counts of coliform organisms, and cultures of the urethral discharge may be positive for gonorrhea and chlamydia. A rapid diagnostic test, such as a NAAT, is now the preferred method for identification of gonorrhea and chlamydia. Treatment Most patients with acute urethritis warrant empiric treatment before the results of laboratory tests are available. Infections caused by coliforms usually respond to the antibiotics described later for treatment of asymptomatic bacteriuria and cystitis. If gonococcal infection is suspected give IM ceftriaxone (250 mg in a single dose) plus 1000 mg oral azithromycin. If the patient is allergic to β-lactam antibiotics, an effective alternative is azithromycin 2000 mg orally in a single dose. This high dose of azithromycin is more likely to be associated with gastrointestinal side effects. An alternative choice in the penicillin-allergic patient is ciprofloxacin 500 mg orally in a single dose. Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 22 If chlamydial infection is suspected or confirmed, the patient should be treated with azithromycin 1000 mg in a single dose. Asymptomatic Bacteriuria and Acute Cystitis The prevalence of asymptomatic bacteriuria in pregnancy is 5% to 10% & the frequency of acute cystitis in pregnancy is 1% to 3%. Some cases of cystitis arise de novo, whereas others develop as a result of failure to identify and treat asymptomatic bacteriuria. Etiology E. coli is responsible for at least 80% of cases of initial infections and about 70% of recurrent cases. Klebsiella pneumoniae and Proteus species also are important pathogens, particularly in patients who have a history of recurrent infection. Up to 10% of infections are caused by gram-positive organisms such as GBS, enterococci, and staphylococci. All pregnant women should have a urine culture at their first prenatal appointment to detect preexisting asymptomatic bacteriuria. If the culture is negative, the likelihood of the patient subsequently developing an asymptomatic infection is less than 5%. If the culture is positive (defined as >105 colonies/mL urine from a midstream, clean catch specimen), prompt treatment is necessary to prevent ascending infection. In the absence of effective treatment, about one third of pregnant women with asymptomatic bacteriuria will develop acute pyelonephritis. Diagnosis Hx Patients with acute cystitis usually have symptoms of frequency, dysuria, urgency, suprapubic pain, hesitancy, and dribbling. Gross hematuria may be present, High fever and systemic symptoms are uncommon. Lab Urine analysis positive leukocyte esterase and nitrate tests Urine culture from a catheterized sample is preferred because it minimizes the probability that urine will be contaminated by vaginal flora. Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 23 With a catheterized specimen, a colony count greater than 102/mL is considered indicative of infection. Treatment Asymptomatic bacteriuria and acute cystitis characteristically respond well to short courses of oral antibiotics. Single dose therapy is not as effective in pregnant women as in nonpregnant patients. However, a 3days course of treatment appears to be comparable to a 7 to 10days regimen for an initial infection. Longer courses of therapy are more appropriate for patients with recurrent infections. In recent years, 20% to 30% of strains of E. coli and more than half the strains of Klebsiella have developed resistance to ampicillin. When choosing among the drugs listed in the table above you should consider several factors. First, the sensitivity patterns of ampicillin, amoxicillin, and cephalexin are the most variable. Second, these drugs—along with amoxicillin-clavulanic acid—also have the most pronounced effect on normal bowel and vaginal flora and thus are the most likely to cause diarrhea or monilial vulvovaginitis. Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 24 o In contrast, nitrofurantoin monohydrate has only minimal effect on vaginal and bowel flora. Moreover, it is more uniformly effective against the common uropathogens, except for Proteus species, than trimethoprim- sulfamethoxazole (TMP-SMX). Third, amoxicillin-clavulanic acid and TMP-SMX usually are the best empiric agents for treatment of patients with suspected drug resistant pathogens. However, sulfonamides should be avoided in the first trimester of pregnancy because of possible teratogenicity, and they should be avoided immediately prior to deliver because of concern about displacement of bilirubin from protein binding sites, with resultant neonatal jaundice Follow up Cultures during or immediately after treatment are indicated for patients who have a poor response to therapy or who have a history of recurrent infection. During subsequent clinic appointments, the patient’s urine should be screened for nitrites and leukocyte esterase. If either of these tests is positive, repeat urine culture and retreatment are indicated. Acute Pyelonephritis The incidence of pyelonephritis in pregnancy is 1% to 2%. Most cases develop as a consequence of undiagnosed or inadequately treated lower urinary tract infection. What predispose pregnant ladies to ascending infection of the urinary tract? First, the high concentration of progesterone secreted by the placenta has an inhibitory effect on ureteral peristalsis. Second, the enlarging gravid uterus often compresses the ureters, particularly the right, at the pelvic brim, thus creating additional stasis. Stasis, in turn, facilitates migration of bacteria from the bladder into the ureters and renal parenchyma About 75% to 80% of cases of pyelonephritis occur on the right side, 10% to 15% are left sided, and slightly smaller percentages are bilateral. Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 25 Etiologies E. coli is again the principal pathogen. K. pneumoniae and Proteus species also are important causes of infection, particularly in women with recurrent episodes of pyelonephritis. Highly virulent gram-negative bacilli such as Pseudomonas, Enterobacter, and Serratia are unusual isolates except in immunocompromised patients. Gram-positive cocci do not frequently cause upper tract infection. Anaerobes also are unlikely pathogens unless the patient is chronically obstructed or instrumented. Diagnosis Hx=> most patients will have fever, chills, flank pain and tenderness, urinary frequency or urgency, hematuria, and dysuria. o Patients also may have signs of preterm labor, septic shock, and acute respiratory distress syndrome (ARDS). Urinalysis=> is usually positive for white blood cell casts, red blood cells, and bacteria. Urine culture=> Urine colony counts greater than 102 colonies/mL in samples collected by catheterization confirms the diagnosis of infection. Treatment Outpatient treatment If their disease manifestations are mild, they are hemodynamically stable, and they have no evidence of preterm labor. The patient should be treated with agents that have a high level of activity against the common uropathogens. o Acceptable oral agents include Augmentin 875 mg twice daily or double- strength TMP-SMX (Cotrimoxazole) twice daily for 7 to 10 days. o Although an excellent drug for lower tract infections, nitrofurantoin monohydrate does not consistently achieve the serum and renal parenchymal concentrations necessary for successful treatment of more serious infections. Inpatient treatment If patient appear to be moderately to severely ill or who show any signs of preterm labor should be hospitalized Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 26 Start IV antibiotic therapy and supportive treatment o They should be monitored closely for complications such as sepsis, ARDS, and preterm labor. o One reasonable choice for empiric IV antibiotic therapy is ceftriaxone 2 g every 24 hours. If the patient is critically ill or is at high risk for a resistant organism, a second antibiotic, such as gentamicin (7 mg/kg/ideal body weight every 24 hours) or aztreonam (500 mg to 1 g every 8 to 12 hours) should be administered, along with ceftriaxone, until the results of susceptibility tests are available. o Once antibiotic therapy is initiated, about 75% of patients’ defervesce within 48 hours. By the end of 72 hours, almost 95% of patients are afebrile and asymptomatic. The two most likely causes of treatment failure are a resistant microorganism and obstruction o obstruction is best diagnosed with CT scan or renal U/S Once the patient has begun to defervesce and her clinical condition has improved, she may be discharged from the hospital. Oral antibiotics should be prescribed to complete a total of 7 to 10 days of therapy. Follow up A repeat urine culture should be obtained after therapy is completed to ensure that the infection has been adequately treated. About 20% to 30% of pregnant patients with acute pyelonephritis develop a recurrent urinary tract infection later in pregnancy. o The most cost effective way to reduce the frequency of recurrence is to administer a daily prophylactic dose of an antibiotic such as nitrofurantoin monohydrate 100 mg. o Patients receiving prophylaxis should have their urine screened for bacteria at each subsequent clinic appointment. They also should be questioned about recurrence of symptoms. o If symptoms recur, or the dipstick test for nitrite or leukocyte esterase is positive, a urine culture should be obtained to determine whether retreatment is necessary. Rh alloimmunization See chapter 9 Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 27 Chapter 2 Antenatal Assessment of Fetal Well Being Prepared by Dr. Amanuel Tefera (MI) Introduction The goal of evidence-based antepartum fetal evaluation is to decrease: perinatal mortality permanent neurologic injury through judicious use of reliable and valid methods of fetal assessment In animals and humans, FHR pattern, level of activity, and degree of muscular tone are sensitive to hypoxemia and acidemia. Redistribution of fetal blood flow in response to hypoxemia may result in diminished renal perfusion and oligohydramnios. Surveillance techniques such as cardiotocography, real-time ultrasonography, and maternal perception of fetal movement can identify the fetus that may be undergoing some degree of uteroplacental compromise. Identification of suspected fetal compromise provides the opportunity to intervene before progressive metabolic acidosis results in fetal death. Causes of fetal death (Stillbirth) Antepartum fetal death is attributed to: - Asphyxia (IUGR, prolonged gestation) =>in about 30% Maternal complications (placental abruption, hypertension, preeclampsia, and diabetes mellitus) => in about 30% Congenital malformations and chromosome abnormalities => in about 15% Infections => 5% No obvious fetal, placental, maternal, or obstetric etiology => in about 20% o this percentage increases with advancing gestational age Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 28 Fetal States To be able to diagnose suspected fetal compromise using tests of fetal biophysical state, blood flow, and heart rate, we must be able to appreciate how these parameters appear under normal conditions and in response to suboptimal conditions. Four normal fetal states have been identified. I. State 1F – Quite sleep state III. State 3F Fetus spends 25% of its time Continues eye movement in the Narrow oscillation of FHR absence of FM Slow FHR, reduced variability No acceleration of FHR with Can last 20Min. movement Existence is questioned II. State 2F- Active sleep state IV. State IV- awake state Fetus spends 60-70% of its time Vigorous body movement Frequent gross movement. Continues eye movement wider oscillation of FHR, FHR acceleration and inc variability Continuous eye movement, Increase variability, and Increase acceleration with FM Can last 40min State 1F and 2F can be affected by activity, drugs & nutritional status Near term, periods of quiet sleep may last 20 minutes, and those of active sleep, about 40 minutes. The mechanisms that control these periods of rest and activity in the fetus are not well established. External factors such as the mother’s activity, her ingestion of drugs, and her nutrition may play a role. Specific factors that may decrease fetal movement in the third trimester include: Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 29 fetal anomalies, particularly central nervous system (CNS) anomalies; maternal exposures, including corticosteroids, sedatives, smoking, and anxiety; low amniotic fluid volume; and decreased placental blood flow due to placental insufficiency When evaluating fetal condition using the NST or the biophysical profile (BPP), the clinician must consider whether a fetus who is not making breathing movements or showing accelerations of its baseline heart rate is in a quiet sleep state or is neurologically compromised. In such circumstances, prolonging the period of evaluation usually allows a change in fetal state, and more normal parameters of fetal well-being will appear o VAS (Vibro-Acoustic Stimulation) Fetal movement is a more indirect indicator of fetal oxygen status and CNS function, and decreased fetal movement is noted in response to hypoxemia. However, gestational development of fetal movement must be considered when evaluating fetal well-being as marked by fetal activity. o Periods of absent fetal movement become more prolonged as gestation advances, o Longer than 40 minutes of fetal inactivity at 40 weeks may be a normal finding, compared with less than 10 minutes at 20 weeks and less than 20 minutes at 32 weeks. Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 30 Indications for testing Pregnancy-related conditions Maternal conditions GH / PE Pregestational DM Decreased fetal movement Hypertension Gestational diabetes mellitus (poorly SLE controlled or medically treated) Chronic renal disease Oligohydramnios Antiphospholipid syndrome IUGR Hyperthyroidism (poorly controlled) Late term or postterm pregnancy Hemoglobinopathies (sickle cell, Isoimmunization sickle cell– hemoglobin C, or sickle Previous fetal demise (unexplained cell–thalassemia disease) or recurrent risk) Cyanotic heart disease Monochorionic MG (with significant growth discrepancy) Recommended frequency of testing If the maternal medical condition is stable and test results are reassuring, tests of fetal well-being (NST, BPP, modified BPP, or CST) are typically repeated at weekly intervals; However, in the presence of certain high-risk conditions, some investigators have performed more frequent testing, although the optimal regimen has not been established. Modalities of antepartum testing Fetal movement count Non stress testing Contraction stress testing Biophysical profile Modified biophysical profile Doppler Velocimetry Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 31 Fetal movement count During the third trimester, the human fetus spends 10% of its time making gross fetal body movements and that 30 such movements are made each hour. Periods of active fetal body movement last about 40 minutes, whereas quiet periods last about 20 minutes. Fetal movement appears to peak between 9:00 PM and 1:00 AM, a time when maternal glucose levels are falling. The longest period without fetal movements in a normal fetus was about 75 minutes. The mother is able to perceive about 70% to 80% of gross fetal movements. Maternal factors that may influence the evaluation of fetal movement include: maternal activity, parity, obesity, medications, and psychological factors, including anxiety. The decrease in fetal movement with hypoxemia makes maternal assessment of fetal activity a potentially simple and widely applicable method of monitoring fetal well-being. Methods of FM counting The Cardiff “count-to-10” methods Sadovsky method o mother count FM once/day o mother count FM 2-3x daily (6am to 6pm) o disruption of end capillaries, and vasogenic edema) and hypoperfusion (=> Ischemia, cytotoxic edema and tissue infarction) are suggested in the development 0f neurologic manifestation. Headache, (in 75% of severe PE) o HA usually start from occipital area, because of the cerebrovascular hyperperfusion that has a predilection for the occipital lobes (because of limited sympathetic innervation in these areas). o Frequently improve after MgSO4 Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 64 Visual changes and & temporary blindness (lasting a few hours to a week) o Is rare in PE, but complicates up to 15% of eclamptic cases o Blindness may arise from 3 major areas Visual cortex of occipital lobe, occipital blindness is also called amaurosis fugax (a transient loss of vision in one or both eyes) (from occipital lobe vasogenic edema) Lateral geniculate nuclei Retina, from retinal ischemia, infarction or detachment, it’s called Purtscher Retinopathy Is a hemorrhagic & vasoocclusive vasculopathy, characterized by multiple white retinal patches and retinal hemorrhage, that are associated with severe vision loss Generalized cerebral edema o Usually manifest by mental status changes that vary from confusion to coma. o Is particularly dangerous because fatal transtentorial herniation can result. Cognitive decline o In women with eclamptic pregnancies Clinical manifestations of PE The clinical findings of PE can manifest as either a maternal syndrome or a fetal syndrome Maternal syndrome The maternal syndrome of PE represents a clinical spectrum with major differences between near term PE without demonstrable fetal effects and PE that is associated with low birth weight and preterm delivery. Maternal manifestations include: Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 65 Symptoms o Headache (severe, global type, which is unresponsive to NSAIDs) o Blurring of vision, or less commonly double vision and blindness (from retinal detachment) o Right upper quadrant or Epigastric pain o Swelling of the face or vulva o Vaginal bleeding o Nausea/vomiting o Difficulty of breathing Signs o Elevated BP, (NB, BP could be normal and patient still can have PE) o Facial/generalized edema o Signs of pleural effusion and ascites o RUQ tenderness o Mental status change (confusion to coma, result of cerebral edema) o Hyperreflexia Laboratory findings o Proteinuria o MAHA, Thrombocytopenia o Elevated serum AST/ALT (2x ULN), LDH, creatinine and bilirubin level o Findings of DIC Fetal manifestations include: - Oligohydramnios, FGR, Abruption, Vascular stillbirth and Preterm delivery Prediction and Prevention of PE ACOG recommends the use of only risk factors for identifying women considered to be at risk for PE. There is insufficient data supporting preventive role of nutritional supplements like Ca, vitamin C, D, and E, garlic… Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 66 Currently low dose aspirin is the only recommended preventive measure in women considered to have high risk for PE, (and also for those with two or more of moderate level risk factors) Preventive role of aspirin is due to its preferential inhibition of TXA2 at low dose, correcting/preventing the imbalance of prostacyclin and TXA2 in the pathogenesis of PE. o The rationale for recommending LDA prophylaxis is the theory that the vasospasm and coagulation abnormalities in preeclampsia are caused partly by an imbalance in the TXA2/prostacyclin ratio It should be started preferably before 16wks of gestation (12-28), and continued till delivery. It decreases rate of severe PE and FGR significantly o reduced the risk of PE by an average of 24% o reduced the average risk of preterm birth by 14% o reduced the risk of FGR by 20% Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 67 Complications of PE Maternal Fetal/Neonatal Seizure/Eclampsia Uteroplacental insufficiency DIC o FGR Pulmonary edema o Oligohydramnios Renal failure o Perinatal death Liver failure Consequences of prematurity Stroke Temporary blindness APH Death Chronic cardiovascular complications postpartum Eclampsia Eclampsia is defined as the development of convulsions (generalized tonic-clonic) or unexplained coma during pregnancy or postpartum in patients with signs and symptoms of PE. ACOG defines eclampsia as a new onset tonic-clonic, focal or multifocal seizure in the absence of other causative conditions, such as, Epilepsy, Cerebral arterial ischemia or infarction, ICH and Drug use. Alternative dx must be considered if seizure occurs after 48-72hrs of postpartum or while administration of MgSo4. In the western world, the reported incidence of eclampsia ranges from 1 in 2000 to 1 in 3448 pregnancies. Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 68 Eclampsia can develop antepartum, intrapartum (most of the time) or postpartum (in around 10% of cases, mostly within 48hr of delivery) Late postpartum eclampsia is defined as eclampsia that occurs after 48 hours but before 4 weeks of delivery. Eclampsia that occurs before the 20th week of gestation is generally associated with molar or hydropic degeneration of the placenta with or without a coexistent fetus Diagnosis The diagnosis of eclampsia is secure in the presence of generalized edema, hypertension, proteinuria, and convulsions. 20-38% of women don’t manifest classic signs of PE (HTN and proteinuria) before seizure episode Eclampsia often (in 78-83%, ACOG 2019) is preceded by premonitory signs of cerebral irritation, (signs of impending eclampsia) such as: - Persistent occipital or frontal headache Blurring of vision (blindness is seen in up to 10-15% of eclamptic patients, and it is mainly due to occipital lobe edema) Photophobia Altered mental status Seizure may lead to severe maternal hypoxia, trauma and aspiration pneumonia CT scan or MRI of the brain is not necessary for the diagnosis and management of eclampsia. However, it is indicated for patients with: - Focal neurologic deficit or prolonged coma Atypical presentation o Onset 48hr postpartum o Eclampsia refractory to adequate therapy Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 69 Differential diagnosis for eclampsia (see Gabby 7th Ed, p692) Severity of Eclampsia Eclampsia is considered severe if one or more of the following are present (Eden’s criteria) Coma of 6 or more hours Temp >39oc PR > 120bpm SBP >200mmHg RR >40 >10 convulsions Maternal and fetal outcomes of eclampsia Maternal (with incidence): - PA (7-10%), DIC (7-10%), Pulmonary edema (3-5%), AKI (5- 9%) Aspiration pneumonia (2-3%) and Cardiopulmonary arrest (2 5%) Feta or perinatal: - Prematurity, PA, Severe FGR, Preterm delivery, is about 50% and about 25% occur before 32wks of gestation Prevention of eclampsia Can be: - Primary: by preventing the development and /or progression of PE, Secondary: by using pharmacologic agents that prevent convulsions in women with established PE. Tertiary: by preventing subsequent convulsions in women with established eclampsia Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 70 Some of the recommended preventive therapies include: close monitoring (in-hospital or outpatient), use of antihypertensive therapy to keep maternal BP below a certain level (< severe range or to normal values), timely delivery, and prophylactic use of magnesium sulfate during labor and immediately postpartum in those considered to have PE Prophylactic MgSo4 is recommended only for women who are hospitalized with the established diagnosis of PE. MgSo4 is associated with a significantly lower rate of recurrent seizures and a lower rate of maternal death than that observed with other agents, like diazepam. NB, about 31-87% of eclampsia is considered unpreventable Chronic HTN and Superimposed PE Chronic HTN: Is defined as an elevated BP that is present prior to conception or is diagnosed before 20th week of gestation, or HTN that persist for more than 12wks postpartum. The frequency of chronic hypertension in pregnancy is estimated at 1% to 5%. Women with chronic hypertension are at increased risk for superimposed PE. Maternal and Perinatal Risks Maternal: Increased risk for the development of superimposed PE, PA (0.7% -2.7% in those with mild HTN and 5% -10% in those with severe or high- risk HTN), and FGR Prepared by Graduating Class of Jimma University 2015 E.C (2022/23) Medstar Obstetrics and Gynecology Second Edition 71 Perinatal: perinatal mortality (3-4x greater), premature delivery and a growth restricted infant Superimposed PE The overall rate of superimposed PE is 25% (14% to 28% in mild HTN and 50% to 79% in severe HTN), the rate is not affected by maternal age, race, or presence of proteinuria early in pregnancy. Criteria to diagnose preeclampsia i
