PHYSIOLOGIC OB REVIEW CLINICAL SIGNIFICANCE:CAN BE ENTRAPPED IN A PFANNENSTEILINCISION AND CAUSE LOSS OF SENSATION IN THE AREA Skin LANGER LINES ◦ orientation of dermal fibers ◦ vertical skin incisions more tension, wider scars ◦ low transverse incisions (Pfannenstiel) follow Langer lines; superior cosmetic results Subcutaneous Layer Camper’s fascia › Superficial › predominantly fatty layer Scarpa’s fascia › Deeper › more membranous layer Arcuate Line Cephalad- aponeuroses invest the rectus abdominis bellies above and below Caudal- all aponeuroses lie anterior to the rectus abdominis muscle, and only the thin transversalis fascia and peritoneum lie beneath. EXTERNAL GENERATIVE ORGANS Blood Supply A. Femoral Artery Branches: – skin , subcutaneous layers , mons pubis › superficial epigastric › superficial circumflex iliac › external pudendal B. External Iliac Artery : PUDENDA or VULVA - muscles , fascia all structures visible externally from the pubis to the perineum: › inferior "deep" epigastric vessels › deep circumflex iliac vessels-. MONS PUBIS • mons veneris Hesselbach triangle • fat-filled CLINICAL SIGNIFICANCE: • covered by curly hair ( escutcheon )in a triangular area Direct hernias- Hesselbach triangle LABIA MAJORA Indirect hernias- deep inguinal ring Male homologue: scrotum WHERE round ligaments terminate Outer surface with hair while inner surface without hairs Merge posteriorly ( posterior commissure.) LABIA MINORA Lacks hair follicles,eccrine and apocrine glands MALE HOMOLOGUE-VENTRAL SHAFT OF PENIS many nerve endings 2 lamellae superiorly lower pair: frenulum of the clitoris upper pair: prepuce Inferiorly fourchette. Anterior Abdominal Wall Innervation ILIOHYPOGASTRIC NERVES- suprapubic area ILIOINGUINAL NERVES (L1)- › lower abdominal wall › upper portion of the labia majora › medial portion of the thigh PHYSIO OB REVIEW FEU-NRMF Page 1 CLITORIS VAGINAL OPENING AND HYMEN • Male homologue: penis • PARTS: glans, a corpus, and two crura HYMEN • richly supplied with nerve ending • Elastic collagenous connective tissue • principal female erogenous • Stratified squamous epithelium organ • Hymenal caruncles-remnants after delivery Imperforate hymen CLINICALLY: • Primary amenorrhea,cyclic pelvic pain,bulging mass at the introitus • Management:cruciate incision or excision VESTIBULE • almond-shaped – BOUNDARIES: • Lateral- Hart line • Medial – hymen • Anterior- frenulum • Posterior-fourchette 6 openings: ◦ urethra ◦ vagina VAGINA ◦ ducts of the Bartholin glands (2) Embryology ◦ ducts of the paraurethral glands/skene glands (2) upper portion - müllerian ducts ◦ lower portion - urogenital sinus Vestibular Glands NO GLANDS WITH ABUNDANT VESSELS vesicovaginal septum-(VAGINA AND BLADDER) rectovaginal septum –(VAGINA AND RECTUM) CLINICAL IMPORTANCE) Posterior fornix-(POUCH OF DOUGLAS)surgical access of the peritoneal cavity LATERAL FORNICES-BI MANUAL EXAMINATION TO PALPATE THE ADNEXA 1. BARTHOLIN’S GLANDS – greater vestibular glands • Open distal to the hymenal ring at 5 & 7 o'clock • INFECTION of ducts:BARTHOLINS CYST/ABSCESS 2. PARAURETHRAL GLANDS – Skene glands – Minor vestibular glands – INFECTION:URETHRAL DIVERTICULUM Vestibular Bulbs • Male homologue: corpus spongiosum of the penis • aggregations of veins beneath the bulbocavernosus muscle • CLINICAL SIGNIFICANCE: • CAUSES VULVAR HEMATOMA DURING DELIVERY PHYSIO OB REVIEW FEU-NRMF Page 2 VAGINA BLOOD SUPPLY LYMPHATIC DRAINAGE cervicovaginal branches External.Superficial space – closed compartment 2.Deep space – continuous superiorly with the pelvic cavity CLINICAL SIGNIFICANCE: o INFECTION OR HEMATOMA IN DEEP SPACE CAN SPREAD TO ABDOMINAL CAVITY MUSCLES CUT IN EPISIOTOMY • Levator ani • Central tendon of the perineum • Bulbocavernosus m. • External anal sphincter Development of the internal generative organs POSTERIOR TRIANGLE Contains: Ischiorectal fossa Anal canal Anal sphincter complex Branches of the internal pudendal vessels Pudendal nerve Embryological development PUDENDAL NERVE • Formed by the anterior rami of S2-S4 • Lies posteromedial to the ischial spines PHYSIO OB REVIEW FEU-NRMF Page 3 . • Superficial transverse perineal m. internal and Upper Third of uterine artery and common iliac nodes vaginal artery Middle third inferior vesical arteries Internal iliac nodes middle rectal and Lower third Inguinal nodes internal pudendal arteries PERINEUM Perineal body Blood supply: Internal pudendal artery (inferior rectal artery and posterior labial artery) NERVE SUPPLY-PUDENDAL NERVE LOCATED IN PUDENDAL CANAL ALSO CALLED AS ALCOCKS CANAL ANTERIOR TRIANGLE Urogenital Triangle 1. where OVARIAN vessels traverse uterine artery(from internal iliac OR HYPOGASTRIC) CARDINAL LIGAMENTS ovarian artery(direct branch of aorta) Transverse cervical or Mackendrodt ligament Thick base of the broad ligament ISTHMUS-FORMS THE LOWER UTERINE SEGMENT OF UTERUS UTEROSACRAL LIGAMENTS • posterior supravaginal portion of the cervix to the fascia over Uterus: Myometrium the sacrum • More muscles in the inner wall than the outer wall. (ROUND Uterus LIGAMENT)mesoteres.upper vagina INTERNAL GENERATIVE ORGANS Cervix Majority-collagen. Ligaments: BLOOD SUPPLY:Sampson artery Broad ligament. Nulliparous: fundus= cervix (UTERUS)mesometrium Multiparous:cervix is 1/3 of the total length • 2.5 to 5 cm ROUND LIGAMENTS Rest in a slight depression OVARIAN FOSSA OF WALDEYER Terminate in labium majus. anterior and posterior walls than in the lateral walls LYMPHATICS • CLINICALLY: • Cervix • Interlacing myometrial fibers .infundibulopelvic ligaments PHYSIO OB REVIEW FEU-NRMF Page 4 .Two müllerian (paramesonephric) - MALE HOMOLOGUE: gubernaculum testis DEVELOPS INTO: oviducts uterus.SUSPENSORY LIGAMENT OR INFUNDIBULOPELVIC LIGAMENT– Posterior wall completely covered by serosa – fimbriated end of the fallopian tube to the pelvic Blood supply: wall. (OVARIES)mesovarium.control of bleeding during the – hypogastric nodes third stage of labor • Body of the uterus Uterus: Endometrium – internal iliac and periaortic lymph nodes • Uterine and ovarian arteries arcuate radial spiral/coiled and basal/straight • CLINICALLY: • SPIRAL ARTERIES – RESPONSIVE TO HORMONES FALLOPIAN TUBES PARTS interstitial portion isthmus ampulla infundibulum or fimbriated (fimbria ovarica) Ovaries Childbearing years. elastin and proteoglycan 10% smooth muscle IF WITH MORE MUSCLE CONTENTINCOMPETENT CERVIX Ectocervix – nonkeratinized squamous epithelium BROAD LIGAMENTS Endocervix – columnar epithelium • Drapes over structures : • (FALLOPIAN TUBES)Mesosalpinx.uterovarian.2. If pregnancy occurs (right panel). the corpus luteum (CL) produces estrogen and progesterone. and selection of the dominant ―ovulatory‖ follicle. which prepare the endometrium for implantation. luteinizing hormone (LH) controls theca cell production of androstenedione. the developing blastocyst begins to produce human chorionic gonadotropin (hCG) and rescues the corpus luteum. After ovulation (right panel).000 follicles bind to the same LH-hCG receptor. which diffuses into the adjacent granulosa cells and acts as precursor for estradiol biosynthesis. FSH = follicle-stimulating hormone. Blood supply:ovarian granulosa cell capacity to convert androstenedione to estradiol is Oocytes are located in the CORTEX controlled by follicle-stimulating hormone (FSH). the corpus FOLLICULAR (PREOVULATORY) OVARIAN PHASE luteum forms and both theca-lutein and granulosa-lutein cells respond to LH. If implantation occurs. human chorionic gonadotropin (hCG) rescues the corpus luteum through Rate of depletion of follicle per month until 35 1000 follicles/month their shared LH-hCG receptor. cAMP = cyclic adenosine monophosphate. The theca-lutein cells continue to produce androstenedione. Low-density lipoprotein (LDL) is an years old important source of cholesterol for steroidogenesis. The ovarian-endometrial cycle has been structured as a 28- day cycle. thus maintaining progesterone production. o During the luteal phase (days 14 to 21). whereas Birth 2 million oocytes granulosa-lutein cells greatly increase their capacity to produce progesterone and to convert androstenedione to estradiol. two-gonadotropin principle of ovarian steroid hormone production. FOLLICULAR PHASE Luteal (Postovulatory) Phase Corpus luteum maintained by LH Estrogensecondary RISE at midluteal phase Progesterone peaks in the midluteal phase The two-cell. LH = luteinizing hormone. During the follicular phase (left panel). LH and hCG Puberty 400.9 % Inhibin B( granulosa cells) inhibit FSH only 1 follicle to reach atresia during lifetime maturity Estrogen Surge 34 – 36 hours before ovulation precise predictor of ovulation LH Surge 10 – 12 hours before ovulation o Gonadotropin control of the ovarian and endometrial cycles. The follicular phase (days 1 to 14) is characterized by rising estrogen levels. # of follicles ovulated during 400 follicles the entire reproductive age STAGES OF HUMAN FOLLICULAR DEVELOPMENT EARLY FOLLICULAR PHASE: percentage of follicles which underwent 99. The PHYSIO OB REVIEW FEU-NRMF Page 5 . endometrial thickening. Decidua • Remainder of uterus Parietalis • Fused with capsularis(14-16 weeks)DECIDUA VERA 3 LAYERS OF DECIDUA PARIETALIS AND BASALIS 3 layers 1.IMPORTANT CLINICALLY IN PRE ECLAMPSIA PREVENTION Other Structures Formed Umbilical cord ◦ Originates from the body stalk The Amnion Innermost avascular fetal membrane Provides the tensile strength IN CASE OF INFECTION MAY WEAKENED PROM preterm delivery Amniotic Fluid AF INCREASE UP TO 34 WEEKS then it declines 1. zona compacta zona functionalis 2. Human Corpus Luteum 22 to 25 predecidual transformation of Regresses 9 –11 days after ovulationDECREASED estradiol and extensive coiling and secretions of glands progesterone MENSTRUATION WHAT WILL MAINTAIN THE CORPUS LUTEUMHCG IN CASE OF PREGNANCY PREMENSTRUAL PHASE PROLIFERATIVE PHASE PREMENSTRUAL PHASE EARLY PROLIFERATIVE PHASE: Infiltration of the stroma by polymorphonuclear leukocytes THIN ENDOMETRIUM pseudoinflammatory appearance to the tissue Narrow and tubular glands. avascular glandular hyperplasia extraembryonic fetal membrane increase in stromal ground substance (edema and proteinaceous material).000 ml.with Mitotic figures MENSTRUAL PHASE NO extravascular blood or leukocyte infiltration SEVERE coiling of the spiral arteries hypoxia of the endometriumstasis/ischemia VASOCONSTRICTION most constant and striking event MENSTRUAL BLOOD –MORE OF ARTERIAL BLOOD ACTION OF PROSTAGLANDINS DURING MENSES: Prostaglandin F2 (PGF2) vasoconstrictor myometrial contractions and uterine ischemia- DYSMENORRHEA DECIDUAL STRUCTURES Decidua beneath blastocyst implantation Basalis LATE PROLIFERATIVE PHASE: Decidua • Overlying the enlarging blastocyst Endometrium thickens. 21 to 24 Stroma becomes edematous.Internally. zona basalis gives rise to new endometrium after delivery DECIDUAL HISTOLOGY NITABUCH LAYER-zone of fibroid degeneration ◦ if defective – Placenta accreta Role & Relationship of the Placenta The blood of the mother and baby DOES NOT mix in a HEMOCHORIAL placenta SECRETORY PHASE MATERNAL BLOOD IN THE INTERVILLOUS SPACE BATHE THE EARLY SECRETORY PHASE: SYNCITIOTROPHOBLAST BEFORE IT ENTERS THE ENDOTHELIAL WALL OF THE FETAL CAPILLARIES DATING OF endometrium POSSIBLE histology of the glandular epithelium Blastocyst Implantation 6 – 7 days after fertilization DAY 17 FIRST SIGN OF OVULATION Glycogen accumulates SUBNUCLEAR VACUOLES STAGE AT THE TIME OF IMPLANTATION Trophoblast Differentiation Villous trophoblast Extravillous trophoblast intervillous trophoblast endovascular trophoblast Penetrates the spiral artery lumen . Capsularis • CHORION LAEVE. zona spongiosa 3. at term PHYSIO OB REVIEW FEU-NRMF Page 6 . FETAL RBC PRODUCTION IS NOT INHIBITED PHYSIO OB REVIEW FEU-NRMF Page 7 . hyperthyroidism • HIGH hCG LEVELS • Maternal virilization-30% – Multifetal pregnancy • Diagnosis: Ultrasound of enlarged ovaries with multiple cysts – Erythroblastosis fetalis • Management: self limited. Asymptomatic . sporadic. non-rhythmic.TSH CLINICAL SIGNIFICANCE:DON’T REMOVE • Detected in blood and urine either in pregnancy or in ASYMPTOMATIC OVARIAN TUMORS AT THIS neoplastic disease TIMEABORTION • Early pregnancy produced by syncitiotrophoblast and cytotrophoblast THECA-LUTEIN CYST DUE TO HIGH HCG (hyperreactio luteinalis) Concentration of hCG in Serum and Urine BILATERAL • Detectable in plasma 7 to 9 days after the midcycle LH surge ASSOCIATED WITH • Doubling TIME every 2 days 1.food intake Mediated by: • regulates bone growth and immune function Estrogen and Progesterone • correlated positively with fetal birthweight Human Placental Lactogen • fetal development and growth FAT METABOLISM PREGNANT UTERUS MATERNAL HYPERLIPIDEMIA UTERINE ENLARGEMENT: Increase: lipids. D-isoimmunization.5 at term Mucus plug Iron requuirement is not available from Marernal storage in most women Beading pattern progesterone OPTIMAL INCREASE in maternal erythrocyte VOLUME WILL NOT DEVELOP (Normal) WITHOUT IRON SUPPLEMENTATION WITH MATERNAL ANEMIA. precursor of estrogen synthesis • LDL-cholesterol from maternal plasma for progesterone OVARIES biosynthesis CORPUS LUTEUM HUMAN CHORIONIC GONADOTROPIN (hCG) functions maximally 6-7 weeks Alpha sub unit is similar to FSH. chronic renal failure Significance of Abnormally High or Low hCG levels 6.peak levels 100. apolipoproteins ◦ Stretching and hypertrophy of muscle cells *Fat is deposited mostly in the central rather than peripheral not hyperplasia sites.000 3. STEROIDOGENESIS Syncitiotrophoblast – major site of steroid production Amniotic fluid estrogen Ferning pattern STEROIDOGENESIS IN PREGNANCY • Fetal adrenal secretion of C-19 steroids. Anti-insulin or "diabetogenic" action Hyperinsulinemia 3. mIU/mL 4. Gestational trophoblastic diseases • Maximal levels 8 to 10 weeks’ gestation 2. Maternal lipolysis and increase in the levels of circulating free Mild fasting hypoglycemia fatty acids Postprandial hyperglycemia 2. multiple fetuses 5. ◦ INCREASE Fibrous tissue AND elastic tissue HEMATOLOGICAL CHANGES IN PREGNANCY CONTRACTILITY HYPERVOLEMIA Braxton Hicks ◦ metabolic demands irregular. lipoproteins. painlesss contractions ◦ support the growing placenta & fetus Unpredictable. • 60th and 80th days after the last menses .resolves after (Fetal hemolytic anemia) delivery – Gestational Trophoblastic Disease • Some – hemorrhage into cysts causing abdominal pain – Fetus w/ Down Syndrome – LOW hCG LEVELS PREGNANCY LUTEOMA – Early pregnancy wastage • solid ovarian tumor – Ectopic Pregnancy • maternal virilization. but usually female fetus is NOT affected!!! • WHY?BECAUSE OF THE CAPACITY OF THE PLACENTA TO Human Placental Lactogen (hPL) CONVERT ANDROGEN TO ESTROGEN • Also called human chorionic somatomammotropin or chorionic • Trophoblasts has the capacity to convert androgen and growth hormone androgen-like factors to estrogen – potent lactogenic and growth hormone-like bioactivity CARBOHYDRATE METABOLISM Metabolic Actions of hPL NORMAL PREGNANCY: 1.LH. and intensity 5-25 ◦ protect FROM blood loss mmHg HYPERVOLEMIA after 32-34 week CERVIX SOFTENING OF CERVIX(GOODELS SIGN) ISTHMUS(HEGARS SIGN) CYANOSIS Cervical Eversion HGB: will average 12. Potent angiogenic hormone POST-PRANDIAL HYPERGLYCEMIA IS DUE TO INCREASED PERIPHERAL Relaxin INSULIN RESISTANCE TO ENSURE SUSTAINED POST-PRANDIAL GLUCOSE • myometrial smooth muscle to promote uterine relaxation and SUPPLY TO THE FETUS the quiescence observed in early pregnancy Leptin • secreted by adipocytes INSULIN SENSITIVITY is LOWER in pregnancy to about 45-70% • an anti-obesity hormone . DM. likely Progesterone effect NORMAL PREGNANCY DURATION GASTROINTESTINAL TRACT Prolonged gastric emptying timeconstipation Pyrosis (heartburn) SIGNS AND SYMPTOMS SUBSEQUENT PRENATAL VISITS MONTHLY UP TO 28 WEEKS EVERY 2 WEEKS 28 WEEKS TILL 36 WEEKS WEEKLY THEREAFTER ASSESSMENT OF GESTATIONAL AGE RDA SOUNDS PERCEIVED BY THE EXAMINER OTHER THAN THE FHT Funic (umbilical cord) souffle • Rush of blood in the umbilical arteries • Sharp. URETERAL DILATATION which is greater on the Right side. URINALYSIS in PREGNANCY Glucosuria may not be abnormal. Hematuria is usually a result of contamination. ACID BASE EQUILIBRIUM Hyperventilationdecreased maternal PCO2 transport of carbon DEFINITIONS dioxide from the fetus to the mother and facilitates release of oxygen from maternal blood to the fetus. Proteinuria is abnormal. whistling sound synchronous with fetal pulse Uterine souffle • Rush of blood through dilated uterine vessels • Soft blowing sound that is synchronous with maternal pulse Sounds resulting from fetal movement Maternal pulse Sounds from maternal intestinal peristalsis ULTRASONIC RECOGNITION OF PREGNANCY PHYSIO OB REVIEW FEU-NRMF Page 8 . and is common. acts during embryonic and fetal development administered to a pregnant woman. STRUCTURAL abnormalities ◦ May cause fetal harm. Strandberg-Larsen. BINGE drinking.COMMON CONCERNS This is just a diagram showing you the weeks of development and wPre- implantation period: 2 weeks from implantation to fertlization Embryonic Period Fetal Period Food and Drug Administration Categories for Drugs and Medications Category A: ◦ Studies in pregnant women have not shown an increased risk for fetal abnormalities. azathioprine. ◦ EXAMPLE: rubella vaccine. Valproic acid. and maternal age (Abel. The minimum amount agents of alcohol required to produce adverse fetal consequences is unknown. do not become apparent until Category X: later ◦ This medication is contraindicated in women who are or may become pregnant. Potassium supplementation. 2001. macrolides. ◦ This medication can cause fetal harm when form and function. and an ◦ systemic cortocosteroids. 2012. Binge drinking. and most cephalosporins Category C: ◦ Animal reproduction studies have shown that this medication is teratogenic (Or embryocidal or has other adverse effect). Phenytoin. Category B: ◦ Animal studies have shown an adverse effect. captopril. anuria oligohydramnios lungs & limbs Disrupt the Fetal Renin-Angiotensin system that is essentail in normal Renal development PHYSIO OB REVIEW FEU-NRMF Page 9 . is believed to pose particularly high risk for alcohol-related birth defects and has also been linked to an increased risk for stillbirth (Centers for Disease Control. ◦ Examples :Levothyroxine.high risk for birth defects and increased risk for Hadegens and trophogens generally affect processes occurring after stillbirth organogenesis or even after birth Dose Effect Chemical or physical exposures that act as hadegens or trophogens are Fetal vulnerability to alcohol is modified by genetic factors. TERATOGEN ◦ Approximately two thirds of all medications are in this category. Many congenital abnormalities. 1995). Maier. association with a specific prenatal exposure is likely to be suspected Carbamazepine. however. Teratogen: may be defined as any agent that acts during embryonic or Category D: fetal development to produce a permanent alteration of form or function. such as penicillins. HADEGEN AFFECTS THE FUNCTION of an organ Features of Fetal Alcohol Syndrome TROPHOGEN Minimum amount of alcohol to produce adverse fetal an agent that alters GROWTH consequences is UNKNOWN. lisinopril prolonged fetal hypotension and hypoperfusionrenal ischemia. and Prenatal multivitamins . much harder to document nutritional status. most major structural anomalies are easily recognized at birth. when taken at recommended doses. renal tubular dysgenesis. ACE Inhibitors and ARBs Enalapril. environmental factors. but adequate and well controlled studies in pregnant women have failed to demonstrate a risk to the fetus ◦ Examples include many antibiotics. 2008). and Lithium. coexisting maternal For simplification. most use the word teratogen to refer to all three types of disease. however. and there are no adequate and well controlled studies in pregnant women. concerns regarding fetotoxicity have been generalized to include this entire medication class. but these observations have not May be concentrated in large fishes been corroborated. Despite theoretical Frontal . The drug may GESTATIONAL AGE OR MENSTRUAL AGE also decrease fetal urine production and thereby reduce time elapsed since the first day of the last menstrual period amnionic fluid volume. 90% chance of survival without physical or neurological impairment. it is recommended that ACE inhibitors and FDA recommendation: DO NOT EAT: shark.to threefold increased risk for cardiac and central microcephaly and severe brain damage nervous system abnormalities. abnormal facies. experience has accrued regarding their Cochlear function .between the frontal and parietal bones prenatal exposure have been identified. and no congenital defects resulting from Coronal .22 and 25WEEKS general safety. Constriction of fetal ductus arteriosus 2. Normal renal development depends on the fetal renal-angiotensin system. centers of ossification Fortunately. most of the commonly used antimicrobial agents are considered safe for 28 Gestatational weeks the embryo/fetus. no adverse effects have Sagittal . ◦ an ashen-gray color ◦ vascular collapse Nitrofurantoin Hyperbilirubinemi a in G6PD deficiency Sulfonamides . long.between the posterior margins of the parietal bones and upper margin of the occipital bone Chloramphenicol Gray baby syndrome in preterm neonates ◦ abdominal distention. ductal flow velocity returned to normal in all external genitalia are fetuses following discontinuation of therapy. With a few exceptions cited below.Hyperbilirubinemia of a preterm infant Tetracyclines yellowish brown discoloration of deciduous teeth PHYSIO OB REVIEW FEU-NRMF Page 10 . 16 Gestational Weeks ANTIMICROBIALS gender can be correctly Aminoglycosides determined by experienced observers by inspection of the external gentamicin or streptomycin nephrotoxicity and ototoxicity genitalia Medications used to treat infections are among those most commonly administered during pregnancy. First-trimester ACE-inhibitor exposure was associated developmental delay and mild neurological abnormalities to with a two. whereas oligohydramnios may result in pulmonary hypoplasia and limb contractures Danazol Because angiotensin-receptor blockers have a similar virilization mechanism of action. but is a known teratogen certain. skull.between the two frontal bones concern for potential fetal toxicity. Aminoglycosides Preterm infants treated with gentamicin or streptomycin have FETAL HEAD developed nephrotoxicity and ototoxicity. Diethylstilbestrol ACE-inhibitor medication causes fetal hypotension and renal vaginal and cervical intraepithelial neoplasia hypoperfusion. Study in 2006: major congenital anomalies: cardiovascular & Sex Hormones CNS Testosterone and Anabolic Steroids Angiotensin-converting enzyme (ACE) inhibitors are considered virilization and may result in ambiguous genitalia fetotoxic and result in ACE-inhibitor fetopathy. swordfish. resulting in pulmonary hypertension. pulmonary hypertension in the neonate Complications morelikely if the drug is taken >72 hours Limb-reduction defects (es. persistent fetal circulation THALIDOMIDE 3. and cardiac. and joint abnormalities allowance of 5000 IU should be avoided ◦ 3 fold increase for tetralogy of Fallot ◦ Category D Isotretinoin anti-acne medication Anti-inflammatory Agents (NSAIDS) ONE OF THE MOST POTENT TERATOGEN IN COMMON USE Indomethacin and other PG inhibitors SIMILAR TO THALIDOMIDE 1.upper limbs) Importantly. Lambdoid . MERCURY The possible embryotoxicity of these two drug classes is less not a drug. tilefish and more than 6 oz of tuna ANTIFUNGALS RETINOIDS Fluconazole Vitamin A Antley Bixler syndrome vitamin A supplements may be safe during pregnancy ◦ oral clefts.between the two parietal bones been demonstrated. NSAIDs may cause adverse fetal effects when Days 27 to 30: upper limb phocomelia taken in late pregnancy Days 30 to 33: lower limb phocomelia Indomethacin may cause constriction of the fetal ductus arteriosus. It is reasonable to offer specialized Tuna sonography for pregnancies with firsttrimester exposure. Other NSAIDs are beginning to show definitive signs of male or female gender assumed to confer similar risks. with subsequent ischemia and anuria Genital tract abnormalities Reduced perfusion may cause fetal-growth restriction and earlier menopause and breast cancer calvarium maldevelopment. Doses higher than the recommended daily bone. This is presumed due to an increase in 280 days or 40 weeks or 9 1/3 calendar months duration vasopressin levels and vasopressin responsiveness Fetal ductal constriction is more likely when the drug is taken in 12 Gestational Weeks the third trimester for longer than 72 hours’ duration. ◦ respiratory abnormalities. king mackerel & angiotensin receptorblocking drugs be avoided. 20 Gestational Weeks Over the years. Given King mackerel the many therapeutic options for treating hypertension during Tile fish pregnancy. IX. and Fetal Macrosomia Corticosteroids and Fetal Lung Maturation fetal hyperinsulinemia Fetal cortisol is the natural stimulus for lung maturation insulin-like growth factor and fibroblast growth factor Glucocorticosteroids (24-34 weeks) ( betamethasone & dexamethasone ) accelerate fetal lung maturity Sexual Differentiation of the Embryo-Fetus Genetic gender—XX or XY—is established at the time of fertilization.from one parietal boss to the other. PHYSIO OB REVIEW FEU-NRMF Page 11 . vagal stimulation. second trimester extracellular fluid that diffuses through the fetal skin(fetal plasma) After 20 weeks amnionic fluid fetal urine.5 cm reducing surface tension in the alveolus ◦ 5% phosphatidyl ethanolamine Smallest circumference . GIT Gonadal Gender If Y chromosome is present(6 weeks )after conception TESTES Fetal Circulation Umbilical veins oxygenated blood Phenotypic Gender Umbilical arteriesunoxygenated blood WITH TESTES male phenotypic sexual differentiation CRISTA DIVIDENS preferentially shunts the well-oxygenated WITHOUT TESTES female differentiation ensues irrespective of blood through the foramen ovale the genetic gender. 10% . fetal erythrocytes( hemoglobin F) bind to Rarely.5 cm). Immunoglobulin G Incomplete but variable androgenic representation for a fetus Transfer of IgG from the motherPREVENT INFECTION IN predestined to be male. and upper vagina Fetal Blood Hemopoiesis Testosterone yolk sac-first trimester virilization of the external and internal genital anlagen. Growth and differentiation of tissues: lungs.Diameters of the head Meconium Occipitofrontal (11. Androgen exposure of the embryo-fetus is excessive Fetal Coagulation Factors 3. Circulatory changes at birth Fetal Testicular Contributions to Male Sexual Differentiation hypogastric arteries umbilical ligaments Müllerian-inhibiting substance umbilical vein ligamentum teres.XX. Presence of growth factors 5. Female Pseudohermaphroditism lowers the affinity of hemoglobin A for oxygen . K is routinely given to newborn after delivery Category 2. protein S. Hemolytic Disease of the Newborn (resulting from D-antigen The presence of testes or no gonads.protein Glucose.allows musculoskeletal development . Function of the amniotic fluid 1. 2. 1.50 % of adult levels MOST COMMON CAUSE :congenital adrenal hyperplasia CLINICAL APPLICATION: Vit. Maintains temperature 3. Hypoxia stimulates arginine vasopressin (AVP) temporal sutures CONTRACTION OF smooth muscle of the colon defecation Occipitomental (12. FETAL PHYSIOLOGY Amnionic Fluid early pregnancy ultrafiltrate of maternal plasma.corresponding to the plane of the ◦ 4% phosphatidyl inositol suboccipitobregmatic diameter is 32 cm.5 cm).from the chin to the most prominent portion of the occiput. prekallikrein. 1.lipid ◦ 50% dipalmitoylphosphatidylcholine (DPPC) – Circumferences of the head principal active component(lecithin) Greatest circumference of the head.XY karyotype. The karyotype is 46.protection from trauma 2.3-DPG) which Category 1. X. cytomegalovirus.0 cm). Ex. alloimmunization) MOST COMMON CAUSE:ANDROGEN INSENSITIVITY SYNDROME OR REINFENSTEIN SYNDROME Immunoglobulin M IgM is increased in newborns with congenital infection such as Category 3: Dysgenetic Gonads rubella. Cushions the fetus . 4.from the middle of the large Formed by type II Pneumocytes fontanel to the undersurface of the occipital bone 90% . or inadequate Fetal Hemoglobin androgen in one destined to be male. ductus venosus ligamentum venosum prevents the development of uterus. Factors II. or toxoplasmosis Müllerian-inhibiting substance is NOT produced.corresponds to the plane ◦ 8-15% phosphatidylglycerol (PG). liver-mid pregnancy bone marrow-third trimester Genital Ambiguity of the Newborn Excessive androgen action in female fetus . Bitemporal (8. 2. NEONATES BUT CAN BE HARMFUL IN CASE OF: A 46. Ovaries are present. antithrombin and plasminogen. fallopian tube. VII. XI. genital ambiguity indicates true hermaphroditism.the greatest distance between the two 3. averages 34. Surfactant Composition Suboccipitobregmatic (9. oxygen more than hemoglobin A because hemoglobin A binds 2. Müllerian-inhibiting substance is NOT produced.3-diphosphoglycerate (2. Insulin. normal bowel peristalsis in the mature fetus Biparietal (9. protein C.5 cm) .capable of of the occipitofrontal diameter . Male Pseudohermaphroditism Production of müllerian-inhibiting substance.root of the nose to the most dark greenish-black ( biliverdin) prominent portion of the occipital bone. Minimal Nutritive function 4.5 cm) . fetal sleep 4. neurologic depression Sleep cyclicity . Acceleration Late deceleration symmetrical gradual decrease and return of the FHR to the baseline associated with a uterine contraction. visually quantitated as the amplitude of the peak-to-trough in beats per minute (bpm) Examine a 1min segment and determine the highest peak and lowest trough.20 minutes -75 minutes 3. The nadir of the deceleration occurs at the same time as the peak of the contraction. Significance: HEAD COMPRESSION Baseline variability Fluctuations in the baseline FHR. The nadir of the deceleration occurs after the peak of the contraction. maternal cigarette smoking) Best practice recommendations ◦ ACOG (2002): Daily fetal movement count after 28 DECELERATIONS DURING NON STRESS TESTING weeks' gestation. Test of fetal condition Neither normal ovaries nor testes are present INTERPRETATION: MOST COMMON CAUSE :TURNERS SYNDROME(46X) Reactive NST-at least 2 accelerations of 15 beats per min PHENOTYPICALLY FEMALE WITH SEXUAL INFANTILISM lasting for 15 secs in a 20 min observation INTERVAL OF TESTING:7 DAYS UNLESS HIGH RISK Category 4: True Hermaphroditism both ovarian and testicular tissues. Fetal androgen exposure is variable. Significance: UTEROPLACENTAL INSUFFICIENCY PHYSIO OB REVIEW FEU-NRMF Page 12 . Repetitive variable decelerations do an ultrasound to check ◦ Perception of 10 distinct movements in 2 hours is for the amount of amniotic fluid volume considered reassuring. PRINCIPLE OF NONSTRESS TESTING NON REACTIVE NST: Sleep – Awake Cycles 1. The karyotype varies among subjects and is commonly Non Stress Test (NST) abnormal. ACOUSTIC STIMULATION TESTS Loud external sounds used to startle the fetus acceleration of the heart rate Positive response fetal heart accelerations following acoustic stimulation Contraction stress test EFM Definition of Terms: Test of uteroplacental function Baseline fetal heart rate Fetal heart rate characteristics in response to uterine Heart rate during a 10min segment rounded to the nearest 5bpm contractions increment Early deceleration EARLY DECELERATION Visually apparent usually symmetrical gradual decrease and return of the FHR to baseline associated with a uterine contraction. medications (magnesium sulfate) Fetal movement counting 5. hypoxia Independent of the maternal sleep-awake state 2. Definitions of the FHR patterns 5 biophysical components BASELINE NORMAL: 110-160 bpm (1) fetal heart rate acceleration (NST) Bradycardia <110bpm (2) fetal breathing Tachycardia >160bpm (3) fetal movements (4) fetal tone A BALANCE between sympathetic & paraS (vagal ) stimulation (5) amnionic fluid volume Under the influence of ARTERIAL CHEMORECEPTORS. THE BIOPHYSICAL PROFILE and biophysical profile The combined use of 5 fetal biophysical variables is a more accurate means of assessing fetal health than a single element. nonstress test.Interpretation of CST SIGNIFICANCE OF AMNIONIC FLUID VOLUME NORMAL VALUE AFI ( 5 – 24 cm) deepest vertical pocket ( 2.increased perinatal morbidity and mortality DOPPLER VELOCIMETRY a non-invasive technique to assess fetal and maternal blood flow BEST TEST FOR IUGR Goal: TO OPTIMIZE TIME OF DELIVERY Sonographic assessment FETAL VESSELS: to determine fetal health and for timely delivery of growth FETAL BIOMETRY monitor lag of growth or absence of growth restricted fetuses BIOPHYSICAL SCORE monitor amniotic fluid and fetal MATERNA VESSELS: to predict placental dysfunction behavior DOPPLER VELOCIMETRY assess the adequacy of blood flow in CURRENT ANTENATAL TESTING RECOMMENDATIONS maternal and fetal vessels There is no "best test" to evaluate fetal well-being (ACOG.low 5 minute apgar score .1999) Three testing systems—contraction stress test.8 cm) Significance of AFI < 5 cm: .hypoxia & hypercapnia modulate rate o 2-5: ULTRASOUND Causes of Fetal Bradycardia Head Compression Congenital Heart Block Fetal Compromise Maternal HypoThermia Causes of Fetal Tachycardia Maternal fever*MOST COMMON Fetal compromise Cardiac arrhythmias Medications: ◦ Parasympathomimetic medications ( Atropine ) ◦ Sympathomimetic ( terbutaline) Baseline FHR variability ABSENT Amplitude range undetectable MINIMAL Amplitude range 5bpm or fewer MODERATE Amplitude range of 6-25bpm MARKED Amplitude range >25bpm NST may be omitted if the 4 ultrasound parameters are all normal PHYSIO OB REVIEW FEU-NRMF Page 13 .increased risk of fetal distress . twin-twin transfusion. repeat within 30 minutes. cord occlusions Cervical examination hemorrhage.20 DELIVER FHR TRACINGS FALL INTO ONE OF THREE CATEGORIES Category • Clearly abnormal requiring immediate action III Category • Indeterminate requiring careful evaluation and possible corrective II measures EARLY Decelerations Nadir of the deceleration occurs at HEAD COMPRESSION the same time as the peak of Category • Clearly normal requiring no change contraction.20. meperidine Vagal blockade (atropine) Defective cardiac conduction system Reduced baseline heart rate variability is the SINGLE MOST RELIABLE SIGN OF FETAL COMPROMISE PROLONGED deceleration Isolated decrease in FHR Definitions of the FHR patterns ≥ 15 bpm. morphine. chorioamnionitis. Maternal acidemia Fetal sleep Prematurity Drugs (MgSO4. AOG Causes of Decreased or Absent Variability Fetal acidemia. peak and end of the recurrent decelerations contraction.25. sine wave like undulating in duration from onset to return to PATTERN Frequency 2-5/minute for ≥ 20 mins baseline Usually assoc with FETAL ANEMIA Causes of Prolonged Deceleration Observed in fetal anemia: Rh Fetal asphxia. nadir and recovery of the Baseline FHR variability UTEROPLACENTAL deceleration occur after the o Absent baseline variability not accompanied by INSUFFICIENCY beginning. observe the fetus is not acidemic at that pH 7.20 . diazepam. movement. time pH is < 7. fetomaternal fetal distress. ≥ 2 minutes but < 10 mins SINUSOIDAL FETAL HEART RATE Smooth.7. o Minimal baseline variability o Marked baseline variability VARIABLE decelerations An ABRUPT decrease in the FHR Accelerations UMBILICAL below the baseline o Absence of induced accelerations after fetal COMPRESSION Less than 30 seconds from onset to stimulation nadir Periodic or episodic decelerations o Recurrent variable decelerations accompanied by minimal or moderate baseline variability o Prolonged deceleration 2 minutes but < 10 minutes o Recurrent late decelerations with moderate baseline variability PHYSIO OB REVIEW FEU-NRMF Page 14 . respectively.Significance of a normal FHR variability Excellent indicator of good fetal well being INCREASED VARIABILITY WITH fetal breathing. another scalp blood sample is collected if < 7. in management I Category I – Normal Baseline rate: 110-160bpm Baseline FHR variability: moderate Late or variable decelarations: absent Early decelerations: present or absent Accelerations: present or absent Category II – Indeterminate Baseline rate: o Bradycardia not accompanied by absent baseline variability o Tachycardia LATE decelerations Onset. butophanol Cord entanglement Maternal supine hypotension Other causes: Conduction analgesia Maternal hypothermia Abruption Umbilical cord prolapse Maternal seizure Valsalva maneuver ACCELERATIONS Visually apparent increase in FHR ≥ 15bpm above baseline lasting ≥ 15 seconds FETAL SCALP BLOOD SAMPLING Accelerations are always Absence of acceleration is not PROTOCOL TO CONFIRM FETAL DISTRESS: reassuring and always confirm that necessarily an unfavorable sign pH > 7.25. Insignificant sinusoidal patterns: Uterine hyperactivity vasa previa bleeding meperidine. Common causes isoimmunization. particular anomalies occur together frequently karyotype. limb contractures. Fetal death a. or both should be considered. Ex: prolonged oligohydramnios->contractures 6. anal atresia. DEFORMATION . limb abnormalities pregnancies affected by trisomy 18 and 21 from unaffected pregnancies PRENATAL DIAGNOSIS OF NEURAL-TUBE DEFECTS Serum markers: Triple Test &Quad Test* NEURAL TUBE DEFECTS (NTD’S) – AFP ◦ second most common class of birth defect – Human chorionic gonadotropin (hCG) ◦ Open neural-tube defects include: – Unconjugated estriol concentration Anencephaly – Dimeric inhibin alpha* Spina bifida Cephalocele Ultrasonographic screening for MINOR ABNORMALITIES Other rare spinal fusion (schisis) Nuchal Translucency (NT) – 1st trimester finding abnormalities Thickened Nuchal Fold – 2nd trimester finding ◦ 95% occur without risk factor or family history Absent nasal bone Space between the 1st and 2nd toes – Sandal gap AMNIOCENTESIS PHYSIO OB REVIEW FEU-NRMF Page 15 . MEASUREMENT IS 3. Family history Treatment of maternal hypotension 2. "overshoots. FIRST TRIMESTER DOWN SYNDROME SCREENING MULTIPLE STRUCTURAL OR DEVELOPMENTAL ABNORMALITIES between 11 and 13 6/7 weeks • SYNDROME .a cluster of several anomalies or defects that have 1. renal anomalies. Example: Spina bifida 2. cardiac defects. Sonographic evaluation: Nuchal translucency (NT) one initial insult • Example: Oligohydramnios leading to pulmonary The American College of Obstetricians and Gynecologists hypoplasia. DISRUPTION a more severe change in form or function DOWN SYNDROME a. NTD – one etiology is a mutation in the MTHFR gene oligohydramnios and with PROM Environmental exposure: hyperthermia. Chromosomal trisomies because of mechanical forces imposed by the uterine 4. GTD environment. anti-folate receptor antibodies AMNIOINFUSION 95% of NTD occur in the absence of risk factors INDICATIONS: Recurrence risk is approximately 4% if a couple previously has a child with prolonged variable decelerations. metabolism. obesity a. Ex: amnionic band causing a cephalocele or limb. 5. fetal but do not seem to be linked etiologically echocardiography. • low maternal serum AFP levels at 15 to 20 weeks reduction abnormality. DM 2. hyperglycemia from IDDM Many women at increased risk for NTD benefit from taking 4mg of FA daily PATTERNS OF UTERINE ACTIVITY: before conception and through the first trimester.20 weeks minutes Normal Value: =/< 2-2.Abnormal Absent FHR variability along with any of the following: o Recurrent late decelerations o Recurrent variable decelerations o Bradycardia o Sinusoidal pattern Associated with abnormal fetal acid-base saturation at the time of observation Maternal O2 RISK FACTORS for NTD’s Discontinue of labor stimulation 1. such as slow return to baseline.an intrinsic abnormality "programmed" in Some Conditions Associated with LOW Maternal Serum AFP development 1.anomalies that all develop sequentially as result of 2.5 MM OR GREATER with a normal fetal • ASSOCIATION . Overestimated gestational age 3. tracheoesophageal • Multiple Maternal Serum Markers could reliably differentiate fistula. medications that disturb folic acid dilute or wash out thick meconium. Montevideo units to define uterine activity Total uterine pressure per contractions in a 10 minute Maternal Serum AFP Screening observation The American College of Obstetricians and Gynecologists (2003) recommends that ALL PREGNANT WOMEN BE OFFERED New Terminology for Uterine Contractions: SECOND-TRIMESTER MATERNAL SERUM AFP SCREENING Normal Uterine Activity: five or less uterine contractions in 10 15 ." or "shoulders" Not predictive of abnormal fetal acid-base status Requires continued surveillance and re-evaluation Do resusitative measures or do ancillary tests to ensure fetal well-being Category III . genetic syndrome or anatomical anomalies associated with Treatment of tachysystole NTDs DELIVER 4. targeted sonographic examination.5 MoM Tachysystole: more than 5 contractions in 10 minutes Abnormal screening test - Genetic Counseling ◦ consideration for a Diagnostic test(ULTRASOUND) ETIOLOGY OF BIRTH DEFECTS 1. and facial (2007b) recommends that when the NUCHAL TRANSLUCENCY deformities. o Variable decelerations with other characteristics. Example: VACTERL association: includes three or more of the following – SECOND TRIMESTER DOWN SYNDROME SCREENING vertebral defects. Maternal serum screening the same cause ◦ free beta hCG • Example: Trisomy 18 ◦ Pregnancy-associated plasma protein A (PAPP-A) • SEQUENCE . environmental agents Change of maternal position 3. high-risk racial or ethnic group 5. MALFORMATION .genetically normal fetus develops abnormally 3. Increased SD ratio (Stuart Index) 3. oligohydramnios sequence. such as Beckwith–Wiedemann or • Transvaginal examination pentalogy of Cantrell Cardiac motion – embryo is 5 mm in length (CRL= 6wks) Renal Agenesis compressed face. Omphalocele • Transabdominal scanning abdominal contents covered only by a two-layered sac of Gestational sac – 6 weeks amnion and peritoneum. Pulsatility index. renal agenesis Potter syndrome.14.OPTIMAL TIME to determine chorionicity bowel herniates into the amnionic cavity • 4.fetal growth EARLY AMNIOCENTESIS • Between 11 and 14 weeks • Same technique • Many centers no longer perform amniocentesis before 14 weeks CHORIONIC VILLUS SAMPLING • 10 to 13 weeks • transcervically or transabdominally.26 weeks most accurate parameter PHYSIO OB REVIEW FEU-NRMF Page 16 . adnexal structures. viability Gastroschisis • 2.4 – 6 weeks Crown-Rump Length(CRL) . Fetal echoes & cardiac activity – 7 weeks The umbilical cord inserts into the apex of the sac part of a genetic syndrome. and cul- survival rate 90 percent de-sac Cause: early vascular occlusionabdominal wall ischemia.BEST TIME to evaluate the uterus.Multifetal gestation . Absence or reversed end diastolic (ARED) blood flow PELVIC ANATOMY Fetal Measurements • LINEA TERMINALIS separates the true and false pelvis Gestational sac (GS) .8-10 weeks Biparietal Diameter (BPD) . 15 and 20 weeks Complications: transient vaginal spotting or amnionic fluid leakage and chorioamnionitis Femur length (FL) . anembryonic gestation / embryonic demise full-thickness defect right of the umbilical cord insertion • 3.variation of 7 to 11 days in the second trimester Abdominal circumference (AC) . Resistance index 4. Complications are similar to those of amniocentesis First Trimester ULTRASOUND Abdominal Wall Defects • 1. DOPPLER VELOCIMETRY Diminished blood flow may be reflected such as the following: 1. Diastolic notch 2. and death from cord compression or pulmonary hypoplasia. 5 cm Posterior sagittal diameter of the outlet* (PSO) – between the tip of the sacrum and the line created by the intertuberous diameter PS: =/> 7. Obstetrical conjugate (OC) • from symphysis pubis to tip of sacrum(4 to 5th sacral ◦ midposition of the symphysis pubis to promontory of vertebrae) the sacrum (2) Interspinous diameter (IS)= 10 cm ◦ • between 2 ischial spines ◦ shortest anteroposterior diameter of the inlet • Smallest pelvic diameter ◦ Measures >/=10 cm (3) Posterior sagittal diameter of the midplane (PSM) ◦ OC= Diagonal conjugate – 1.between 2 ischial tuberosities linea terminalis IT – 11 cm ◦ = 13. True conjugate (TC) Boundaries: ◦ Superior portion of symphysis pubis to promontory of Anterior: undersurface of Pubic Arch the sacrum Posterior . = 12 cm ◦ 3.ISCHIAL SPINES distance between them usually represents the shortest diameter of the pelvic cavity valuable landmarks for fetal head descent PLANES AND DIAMETERS OF THE PELVIS Four Imaginary Planes Plane of the Pelvic Inlet—the Superior strait Plane of the Pelvic Outlet—the Inferior strait Plane of the Midpelvis—the LEAST pelvic dimensions Plane of Greatest Pelvic dimension—of no obstetrical significance PELVIC INLET Boundaries: Posterior: Sacrum -promontory and alae Lateral: Linea terminalis Anterior: horizontal pubic rami and the symphysis pubis Shape: round or gynecoid in 50 % of white women MIDPELVIS (Plane of least pelvic dimension) • Boundaries: Anterior .tip of the Sacrum ◦ N.5-2 cm = 4.5 cm ◦ greatest transverse diameter (GTI) .2cm Anteroposterior diameter of the outlet (APO) – undersurface of pubic arch to tip of the sacrum B.inferior portion of symphysis pubis Lateral .Ischial spines Posterior – tip of sacrum A. Anteroposterior Diameter (1) AnteroPosterior diameter (APM) = 11.V.5-11.5 cm 1.5 cm • between sacrum and the line created by the interspinous diameter PELVIC OUTLET 2. = 11 cm Lateral: Sacrosciatic ligaments & the Ischial tuberosities ◦ TC= Diagonal conjugate-1.V.distance between the Intertuberous diameter (IT) . Diagonal conjugate (DC) ◦ lower margin of the symphysis to the promontory of the sacrum ◦ N.5 cm PELVIC SHAPES Caldwell and Moloy classification Posterior segment determines the type of pelvis Anterior segment determines the tendency Many pelvis are not pure but are mixed PHYSIO OB REVIEW FEU-NRMF Page 17 . Transverse diameter AP: 9. it is usually engaged EXCEPT if there is molding or Stage of placental separation and caput formation expulsion Begins after delivery of the fetus and ends PELVIC OUTLET MEASUREMENTS with the delivery of the placenta Intertuberous diameter (IT) = >8cm 2 Phases of cervical dilatation: Distance between two ischial tuberosities ◦ Latent phase Place a closed fist against the perineum between two ischial variable and sensitive to extraneous tuberosities factors .‖ Phase 3 of Parturition: Labor Stages of Labor ◦ First stage Stage of cervical effacement and dilatation Ends when the cervix is fully dilated( 10 Engagement cm) Descent of the biparietal plane of the fetal head to a level ◦ The Second stage below that of the pelvic inlet Stage of fetal expulsion IF HEAD is engaged the INLET is adequate Begins when cervical dilatation is ascertained by vaginal exam and by abdominal palpation complete(10cms) and ends with delivery When the lowermost portion of the fetal head is at or below the ◦ Third stage of labor ischial spines. sedation and myometrial stimulation Midpelvis Estimation ◦ Active phase Suspicious findings for MIDPELVIC CONTRACTION Acceleration phase Prominent ischial spines predictive of the outcome of a sidewalls are convergent particular labor shallow concavity of the sacrum PHYSIO OB REVIEW FEU-NRMF Page 18 . described by women as ―THE BABY DROPPED. Ex: a Gynecoid pelvis with an android tendency PHASES OF PARTURITION Gynecoid suited for delivery of most fetuses found in almost 50 percent of women Anthropoid oval anteroposteriorly > AP diameter than Transverse diameter Android poor prognosis for vaginal delivery Phase 1 of Parturition: Uterine Quiescence and Cervical Softening Uterine Quiescence Platypelloid ◦ Braxton Hicks contractions or False labor Short AP and wide Transverse diameters Low-intensity myometrial contractions felt by the mother but DO NOT cause cervical dilatation Phase 2 of Parturition: Preparation for Labor LIGTHENING ◦ Abdomen undergoes a shape change. retracts and expels fetus BREECH PRESENTATION Frank Breech – thighs are flexed and the legs extended LOWER SEGMENT: Complete Breech – thighs AND legs are flexed Softer . (2) compression of nerve ganglia (3) cervical stretching (4) stretching of the peritoneum Ferguson reflex ◦ Manipulation of the cervix and ―stripping‖ the fetal membranes cause the release of prostaglandin F2α metabolite (PGFM) Distinct Lower and Upper Uterine Segments UPPER SEGMENT: firm during contractions contracts.if one or both feet. sinciput and brow presentations almost always (1) hypoxia of the contracted convert into vertex or face presentations by neck flexion or extension.‖ Causes of labor pains: As labor progresses. but dependent on lactation-induced amenorrhea(LAM) FETAL LIE Relation of the long axis of the fetus to that of the mother TYPES: Longitudinal › 99% of labors at term Transverse lie › Predisposing factors: multiparity. L2 and L3 – examiner stands at the side of the bed and faces FETAL PRESENTATION the patient portion of the fetal body foremost within the birth canal L4 – examiner faces patients feet PHYSIO OB REVIEW FEU-NRMF Page 19 .distended and more passive Incomplete. the arms are usually crossed over the thorax or become parallel to the sides. Phase of maximum slope good measure of over – all efficiency of the uterus Deceleration phase reflective of feto-pelvic relationship First Stage of Labor: Clinical Onset of Labor ◦ ―Show‖ or ―bloody show. or one or both knees. hydramnios. blood does not escape externally Fetal membranes appears first at the vulva DUNCAN Separates at periphery blood escapes from the vagina placenta descends sideways (cotyledons)appears first Phase 4 of Parturition: The Puerperium lactogenesis and milk let-down Reinstitution of ovulation Within 4 to 6 weeks after birth. LEOPOLD’S MANEUVER L1. or Footling Breech . with back up or back down. the right or left side of the birth canal. are lowermost or extended Uterine Changes during Labor physiological retraction ring-junction between the lower and upper segment In obstructed labor--> the ring is prominent--> pathological retraction ring or Bandl ring Stages of Labor ◦ 1st Stage of Labor: Clinical Onset of Labor ◦ 2nd Stage of Labor: Fetal Descent ◦ 3rd Stage of Labor: Delivery of Placenta and Membranes MECHANISM OF PLACENTAL SEPARATION: FETAL POSITION SCHULTZE relationship of the chosen portion of the fetal presenting part to Central separation. myometrium respectively. placenta previa. The umbilical cord lies in the space between them DIAGNOSIS OF FETAL PRESENTATION AND POSITION and the lower extremities. and uterine anomalies Oblique Lie › 45-degree angle › unstable Varieties of Presentations and Positions Shoulder presentations( acromion (scapula) is the portion of the FETAL ATTITUDE fetus UNIVERSAL FLEXION Another term used is transverse lie. Extension o More of the ANTERIOR parietal bone presents 6. Descent 3. extension and straightening of the fetal body Flexion suboccipitobregmatic diameter is substituted for the longer occipitofrontal diameter Internal Rotation occiput gradually moves toward the symphysis pubis anteriorly from its original position PHYSIO OB REVIEW FEU-NRMF Page 20 . the rest of the body quickly Fourth Maneuver – Pelvic grip passes. The latent phase for most women ends at between 3 and 5 cm of dilatation. Expulsion POSTERIOR ASYNCLITISM o Sagittal suture lies close to the symphysis o POSTERIOR parietal bone will present Changes in Shape of the Fetal Head CAPUT SUCCEDANEUM The portion of the fetal scalp becomes edematous MOLDING The change in fetal head shape from external compressive forces Latent Phase Mother perceives regular contractions. External Rotation 7. pressure of the amnionic fluid 2. direct pressure of the fundus upon the breechs 3.First Maneuver – Fundal Grip Extension Breech – sensation of a large. in the presence of follow until the onset of the second stage uterine contractions Multiparous= descent begins with engagement Four forces FOR DESCENT 1. irregular and mobile parts External Rotation bisacromial diameter into relation with the anteroposterior Third Maneuver – Pawlik’s grip diameter of the pelvic outlet The lower portion of the abdomen is grasped just above the symphysis pubis Expulsion Engaged or not engaged anterior shoulder appears under the symphysis pubis. and further descent cervical dilatation of 3 to 5 cm or more. resistant Extremities – numerous small. ANTERIOR ASYNCLITISM 1. resistant pelvic floor Back – hard. After delivery of the shoulders. exerted by the uterus Second Maneuver – Lumbar Grip 2. nodular body Head presses upon the pelvic floor Cephalic –hard and round movable and balottable Two forces : 1. bearing down efforts 4. Flexion ANTERIOR ASYNCLITISM 4. Internal Rotation o Sagittal suture approaches the sacral promontory 5. DETERMINE THE CEPHALIC PROMINENCE Vertex Presentation – the prominence is on the same side as ASYNCLITISM the small parts It is the lateral deflection of the head to a more anterior or Face Presentations – the prominence is on the same side as the posterior position in the pelvis back 2 TYPES OF ASYNCLITISM CARDINAL MOVEMENTS OF LABOR 1. Engagement 2. Prolonged Latent Phase > 20 hours in nullipara CARDINAL MOVEMENTS OF LABOR >14 hours in multipara Descent first requisite for birth of the newborn Active Labor Nulliparas= engagement before labor. POSTERIOR ASYNCLITISM 2. Rapid Labor 2. Sudden gush of blood 3. perineal body and sphincter FIRST STAGE Fourth Degree Laceration Extends through the rectal mucosa to expose the lumen of the Latent Phase <20 hours <14 hours rectum Active Phase 1. labor is likely to occur Not effective by mouth 3. Other Tests : Arborization or ferning pattern Prostaglandins alpha-fetoprotein positive Not used routinely injection of various dyes into amniotic sac management of postpartum hemorrhage due to uterine atony PG F2-NOT USED IN B. prolapse of the umbilical cord Oxytocin (pitocin. THIRD STAGE 15-30 mins 15-30 mins ABNORMAL LABOR PATTERNS. Early detection of meconium staining 3. the use of the indicator Nitrazine SIDE EFFECTS: transient severe hypertension yellow-->blue NOT USED IN PATIENTS WITH BRONCHIAL ASTHMA 4. amniotic fluid pooling Ergonovine and Methylergonovine 2. AND METHODS OF TREATMENT MANAGEMENT OF FIRST STAGE OF LABOR FETAL HEART RATE MONITORING First stage of labor: every 30 minutes (LOW RISK) 15 MINS (HIGH RISK) Second stage: every 15 mins(LOW RISK) 5 MINS (HIGH RISK) Maternal monitoring and management during labor BENEFITS FROM AMNIOTOMY 1. increased incidence of intrauterine infection SIDE EFFECTS: ANTIDIURETIC/HYPOTENSION NOT GIVEN AS IV BOLUS DIAGNOSIS 1. DIAGNOSTIC CRITERIA.5 is consistent with ruptured membranes Powerful stimulants of myometrial contraction 3. Calkin’s Sign – the uterus becomes globular The earliest SIGN to appear. Testing the pH of the vaginal fluid : From ergot pH above 6. syntocinon) 2. ASTHMA STATION PG E2-SAFE FOR BRONCHIAL ASTHMA When lowermost portion of presenting part is at level of ischial spines designated as zero LACERATIONS OF THE BIRTH CANAL Divisions represent cms above and below the spines into fifths First Degree Laceration fourchette. Uterus rises in the abdomen 4. mucous membrane.5cm/hr SECOND STAGE 50 mins 20 mins PHYSIO OB REVIEW FEU-NRMF Page 21 . 2. AND METHYLERGONOVINE DETECTION OF RUPTURED MEMBRANES SIGNIFICANCE OXYTOCIC AGENTS 1. Opportunity to apply electrode RITGEN MANUEVER OR MODIFIED RITGEN MANUEVER Pressure on the chin of the fetus through the perineum . the other hand exerts pressure superiorly against the occiput Factors contributing to both protraction and arrest disorders excessive sedation epidural analgesia fetal malposition Signs of placental separation 1. Lengthening of the umbilical cord Delivery of the Placenta Traction on the umbilical cord must not be used to pull the placenta out of the uterus---> UTERINE INVERSION Active management of the 3rd stage UTERINE MASSAGE OXYTOCIN. perineal skin and vaginal mucous membrane DURATION OF STAGES OF LABOR Second Degree Laceration skin and mucous membrane.2cm/hr 1. ERGONOVINE. the fascia and muscles Nullipara Multipara Third Degree Laceration skin. amino acid. methylergonovine.8 to 39°) arrest or retardation of involution Causes: Treatment: binder or brassiere. minerals. LOCHIA SEROSA. fever and tachycardia.Escherichia coli infections contains both T and B lymphocyte Dyspareunia Rare Occasional LACTATION INHIBITION Milk leakage. Superficial layer Hepatitis C infection is not a contraindication to breast feeding ◦ BECOMES NECROTIC--> sloughed in the lochia Herpes simplex virus if there are no breast lesions is NOT a Basal layer contraindication to breast feeding ◦ adjacent to the myometrium--> the source of new endometrium BREAST FEVER breasts -->distended. and breast pain ( 3 to 5 days) Extensions Common Uncommon TREATMENT: Ice packs analgesics PUERPERIUM Bromocriptine . and reassurance ◦ retention of a placental fragments Mild and self-limited to 2 to 3 days. c ◦ uterus is larger and softer Immediate source of organisms --> infant's nose and throat Management of Subinvolution TREATMENT: MASTITIS ◦ Ergonovine or methylergonovine culture of the expressed milk ◦ Antibiotic therapy for infection antimicrobial therapy: ◦ Chlamydia trachomatis ◦ Dicloxacillin 500 mg orally four times daily.degree of depressed mood a few days after delivery 6 weeks ◦ Excitement and fears during pregnancy and delivery ◦ Complete extrusion of the placental site ◦ Discomforts of the early puerperium ◦ Fatigue from loss of sleep during labor and postpartum LATE POSTPARTUM HEMORRHAGE ◦ anxiety over the ability to provide appropriate infant care. firm. for lactation inhibition is associated with considered to be between 4 and 6 weeks strokes. pumping of the breast ◦ Infection ◦ retained placental fragments MASTITIS ◦ incompletely remodeled uteroplacental arteries unilateral.After about the 10th day. and psychiatric disturbances. and nodular SUBINVOLUTION elevation of temperature (ranged from 37. inflammation.protein but less sugar and fat Faulty hearing Rare More common HUMAN MILK Postoperative Minimal Common All vitamins EXCEPT VIT K are found in human milk pain Vitamin K after delivery is required to prevent hemorrhagic disease of the newborn Anatomical Excellent Occasionally results faulty IMMUNOLOGICAL CONSEQUENCES OF BREASTFEEDING Blood loss Less More SECRETORY IgA less prone to enteric infection against rotavirus infections. WHITE or YELLOWISH WHITE color CONTRAINDICATIONS TO BREASTFEEDING Breastfeeding is not contraindicated if hepatitis B immune DECIDUA AND ENDOMETRIAL REGENERATION globulin is given to infants of seropositive mothers. although it sometimes lasts Treatment for up to 10 days ◦ oxytocin. INVOLUTION OF THE REPRODUCTIVE TRACT UTERINE INVOLUTION CONTRACEPTION FOR BREASTFEEDING WOMEN 4 weeks after delivery Recommendations for Hormonal Contraception if Used by Breast Feeding ◦ uterus regains its previous nonpregnant size Women 1.Hormonal implants -->inserted at 6 weeks postpartum. PALE in color LOCHIA ALBA.first few days after delivery. engorgement. ice bag. ◦ irregular or excessive uterine bleeding ETIOLOGY: Staphylococcus aureus – 40 %. and American College of Obstetricians and Gynecologists (2013b) body image concerns ◦ bleeding 24 hours to 12 weeks after delivery Causes: TREATMENT ◦ MOST COMMON CAUSE: anticipation.NON RESPONSIVE TO medical HOME CARE management COITUS .a LOCHIA RUBRA. seizures. RED color i 3.MIDLINE versus MEDIOLATERAL EPISIOTOMY LACTATION COLOSTRUM Characteristic Midline Mediolateral deep lemon-yellow-colored liquid 2nd postpartum day Surgical repair Easy More difficult rich in immunological components(Ig A).Depot medroxyprogesterone acetate --> 6 weeks postpartum.After 3 or 4 days.no definite time after delivery when coitus should be resumed -coitus may be resumed based on the patient's desire and comfort PHYSIO OB REVIEW FEU-NRMF Page 22 . ergonovine. marked engorgement. menses usually return within 6 to 8 weeks ◦ Suction curettage – large clots ◦ Curettage. myocardial infarctions. recognition. analgesic. MOST COMMON CAUSE ◦ Erythromycin if penicillin sensitive MANAGEMENT: Azithromycin or ◦ Vancomycin is effective against MRSA Doxycycline treatment for 10 to 14 days PLACENTAL SITE INVOLUTION Postpartum blues.Progestin-only oral contraceptives --> started 2–3 weeks postpartum LOCHIA 2. SIGNS AND SYMPTOMS chills. or prostaglandins CONTRACEPTION ◦ Antimicrobial – with infection Not breastfeeding. small mandible. PARACERVICAL BLOCK • Pain relief during the first stage of labor PHYSIO OB REVIEW FEU-NRMF Page 23 . or difficulty opening mouth COMPLICATIONS OF SPINAL (SUBARACHNOID) BLOCK 4. tachycardia. placenta previa or higher-order multiple gestation • Increased intracranial pressure EPIDURAL ANESTHESIA Goals for Optimizing Obstetrical Anesthesia Services Continuous Lumbar Epidural Block Nonpharmacological Methods of Pain Control • VAGINAL DELIVERY . CLINICAL HYPNOSIS – power of the mind to heal the body. Cardiovascular Toxicity Hypertension . neck. or arthritis of the neck • Hypotension • High spinal blockade 5. • Lidocaine or Bupivacaine including trauma or surgery Cesarean Delivery • T4 dermatome 3.g. Goiter • Spinal (Postural puncture) headache • Convulsions 6.. Serious maternal medical problems. Some Local Anesthetic Agents used in Obstetrics) • Ease and rapid/ minimal risk of vomiting • Poor analgesic agents Central Nervous System Toxicity • May cause newborn depression • Bizarre behavior. loss of consciousness • causes a rise in blood pressure • Unpleasant delirium and hallucination. hematoma formation • Morbid obesity is also a major risk factor for failed or difficult from perforation of a blood vessel intubation. ACUPUNCTURE • Hypotension • Central nervous stimulation EFFICACY AND SAFETY OF PARENTERAL AGENTS • Maternal pyrexia 1. Marked Obesity • T10 dermatome 2. Severe edema or anatomical abnormalities of face.T10 to S5 1. LAMAZE • CESAREAN DELIVERY . • Total spinal blockade increases of beta endorphins in the peripheral blood • Ineffective analgesia 3. generalized convulsions. muscle fasciculation and Ketamine excitation. • Lidocaine or Chloroprocaine at 3 and 9 o’clock • Complication: fetal bradycardia ANESTHESIA AND ANALGESIA MATERNAL RISK FACTORS THAT SHOULD PROMPT ANESTHESIA CONSULTATION: SPINAL (SUBARACHNOID) BLOCK Vaginal Delivery • forceps or vacuum delivery 1. Extremely short stature . Bleeding disorders Contraindications to Spinal Anesthesia 8. Obstetrical complications likely lead to operative delivery – • Skin infection e. pulmonary or • Bladder dysfunction neurological disease • Oxytocics and hypertension • Arachnoiditis and meningitis 7. such as cardiac. short neck. hypotension and cardiac INTUBATION arrhythmias • Sellick maneuver – Cricoid pressure is used to occlude the esophagus from induction until intubation PUDENDAL BLOCK • Relatively safe and simple Failed Intubation • Complications: serious systemic toxicity. Abnormal dentition. Severe preeclampsia ABSOLUTE CONTRAINDICATIONS 9. Meperidine is the most common opioid used worldwide for pain • Back pain relief in labor. Previous history of anesthetic complications • hypotension • coagulopathy • bacteremia 10. COMPLICATIONS OF EPIDURAL ANESTHESIA 2. • Meperidine or other narcotics – cause newborn respiratory Effects on Labor depression • Prolongs active phase of labor by 1 hour • Increases the need for instrumental delivery LIKE FORCEPS AND NARCOTIC ANTAGONISTS VACUUM due to prolonged second-stage labor Naloxone • Reverses respiratory depression induced by opioid narcotics Contraindications NITROUS OXIDE • Hemorrhage • 50% nitrous oxide and oxygen provides satisfactory analgesia • during labor • Infection at or near the sites of puncture • REGIONAL ANALGESIA • Suspicion of neurological disease SENSORY INNERVATION OF THE GENITAL TRACT • Anticoagulation Uterine Innervation • Early in labor – SENSORY T11 and T12 nerves • Severe Preeclampsia-Eclampsia • Motor pathways – T7 and T8 vertebrae • BEST ANESTHESIA: EPIDURAL ANESTHESIA Lower Genital Tract Innervation GENERAL ANESTHESIA • Pudendal nerve – sensory nerve fibers from S2 through S4 PATIENT PREPARATION nerves ANTACIDS Passes beneath the posterior surface of the UTERINE DISPLACEMENT sacrospinous ligament just as the ligament attaches • Lateral uterine displacement to the ischial spine Preoxygenation ANESTHETIC AGENTS Thiopental • (Table 19-3. slurred speech. or spine.T4 to S1 • teaching pregnant women relaxed breathing and their labor partners psychological support techniques. • produce remarkable uterine relaxation • USES: Internal podalic version of the second twin Breech decomposition Replacement of acutely inverted uterus . • A fasting period of 8 hours or more is preferable for uncomplicated parturients undergoing elective cesarean delivery. GAS ANESTHETICS Volatile Anesthetics • Most commonly used is isoflurane. . ASPIRATION • Aspiration pneumonitis has been the most common cause of anesthetic deaths in obstetrics. PHYSIO OB REVIEW FEU-NRMF Page 24 . ASPIRATION • Aspiration pneumonitis has been the most common cause of anesthetic deaths in obstetrics. FASTING • A fasting period of 8 hours or more is preferable for uncomplicated parturients undergoing elective cesarean delivery.