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PHYSIOLOGIC PHYSIOLOGIC OB REVIEW
CLINICAL SIGNIFICANCE:CAN BE ENTRAPPED IN A PFANNENSTEIL INCISION 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 abd ominis 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 skin , subcutaneous layers , mons pubis superficial epigastric epigastric › superficial circumflex circumflex iliac › external pudendal › B. External Iliac Artery : - muscles , fascia inferior "deep" epigastric vessels › deep circumflex iliac vessels-. › Hesselbach triangle CLINICAL SIGNIFICANCE: Direct hernias- Hesselbach triangle Indirect hernias- deep inguinal ring
PUDENDA or VULVA all structures visible externally from the pubis to the perineum: perineum: MONS PUBIS mons veneris fat-filled covered by curly hair ( escutcheon )in a triangular area LABIA MAJORA Male homologue: scrotum WHERE round ligaments 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 frenulum of the clitoris upper pair: prepuce pair: prepuce Inferiorly fourchette. fourchette. • •
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Anterior Abdominal Wall Innervation ILIOHYPOGASTRIC ILIOHYPOGASTRIC NERVES- suprapubic area ILIOINGUINAL NERVES (L 1) lower abdominal wall › upper portion of the labia majora › medial portion of the thigh › PHYSIO OB REVIEW FEU-NRMF
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VAGINAL OPENING AND HYMEN Male homologue: penis penis PARTS: glans, a corpus, and two crura richly supplied with nerve ending principal female erogenous organ •
HYMEN •
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Elastic collagenous connective tissue Stratified Stratified squamous epithelium Hymenal caruncles-remnants after delivery
Imperforate hymen CLINICALLY: Primary amenorrhea,cyclic pelvic pain,bulging mass at the introitus Management:cruciate incision or excision •
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VESTIBULE •
almond-shaped BOUNDARIES: Lateral- Hart line Medial – Medial – hymen hymen Anterior- f renulum Posterior-fourchette 6 openings: urethra ◦ vagina ◦ ducts of the Bartholin glands (2) ◦ ducts of the paraurethral glands/s kene glands (2) ◦ –
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VAGINA
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Vestibular Glands
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Embryology upper portion - müllerian ducts lower portion - urogenital sinus NO GLANDS WITH ABUNDANT VESSELS vesicovaginal septum-(VAGINA AND BLADDER) rectovaginal septum – septum – (VAGINA (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
BARTHOLIN’S GLANDS greater vestibular glands Open distal to the hymenal ring at 5 & 7 o'clock INFECTION of ducts:BARTHOLINS ducts:BARTHOLINS CYST/ABSCESS –
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PARAURETHRAL GLANDS Skene glands Minor vestibular glands glands INFECTION:URETHRAL INFECTION:URETHRAL DIVERTICULUM – – –
Vestibular Bulbs Male homologue: corpus spongiosum of the penis aggregations of veins beneath the bulbocavernosus muscle muscle CLINICAL SIGNIFICANCE: CAUSES VULVAR HEMATOMA DURING DELIVERY •
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VAGINA BLOOD SUPPLY
LYMPHATIC DRAINAGE
Upper Third
cervicovaginal branches of uterine artery and vaginal artery
External, internal and common iliac nodes
Middle third
inferior vesical arteries
Internal iliac nodes
Lower third
middle rectal and internal pudendal arteries
Inguinal nodes
PERINEUM 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
Perineal body
ANTERIOR TRIANGLE Urogenital Triangle 1.Superficial space – closed compartment 2.Deep space – continuous superiorly with the pelvic cavity CLINICAL SIGNIFICANCE: INFECTION OR HEMATOMA IN DEEP SPACE CAN o SPREAD TO ABDOMINAL CAVITY MUSCLES CUT IN EPISIOTOMY Levator ani Central tendon of the perineum Bulbocavernosus m. Superficial transverse perineal m. External anal sphincter •
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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 •
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Two müllerian (paramesonephric) DEVELOPS INTO: oviducts uterus,upper vagina
MALE HOMOLOGUE: gubernaculum testis
INTERNAL GENERATIVE ORGANS
Cervix
Majority-collagen, elastin and proteoglycan 10% smooth muscle IF WITH MORE MUSCLE CONTENT INCOMPETENT CERVIX Ectocervix – nonkeratinized squamous epithelium Endocervix – columnar epithelium
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Uterus
BROAD LIGAMENTS Drapes over structures : (FALLOPIAN TUBES) Mesosalpinx, (ROUND LIGAMENT) mesoteres, (OVARIES) mesovarium, (UTERUS) mesometrium 2.SUSPENSORY LIGAMENT OR INFUNDIBULOPELVIC LIGAMENT – fimbriated end of the fallopian tube to the pelvic wall, where OVARIAN vessels traverse CARDINAL LIGAMENTS Transverse cervical or Mackendrodt ligament Thick base of the broad ligament UTEROSACRAL LIGAMENTS posterior supravaginal portion of the cervix to the fascia over the sacrum
Nulliparous: fundus= cervix Multiparous:cervix is 1/3 of the total length Posterior wall completely covered by serosa Blood supply: uterine artery(from internal iliac OR HYPOGASTRIC) ovarian artery(direct branch of aorta)
ISTHMUS-FORMS THE LOWER UTERINE SEGMENT OF UTERUS Uterus: Myometrium More muscles in the inner wall than the outer wall, anterior and posterior walls than in the lateral walls CLINICALLY: Interlacing myometrial fibers - control of bleeding during the third stage of labor Uterus: Endometrium Uterine and ovarian arteries arcuate radial spiral/coiled and basal/straight CLINICALLY: SPIRAL ARTERIES – RESPONSIVE TO HORMONES •
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LYMPHATICS Cervix •
hypogastric nodes Body of the uterus internal iliac and periaortic lymph nodes –
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FALLOPIAN TUBES PARTS
interstitial portion isthmus ampulla infundibulum or fimbriated (fimbria ovarica)
Ovaries
ROUND LIGAMENTS Terminate in labium majus. BLOOD SUPPLY:Sampson artery PHYSIO OB REVIEW FEU-NRMF
Childbearing years- 2.5 to 5 cm Rest in a slight depression OVARIAN FOSSA OF WALDEYER Ligaments: Broad ligament,uterovarian,infundibulopelvic ligaments Page 4
Blood supply:ovarian Oocytes are located in the CORTEX FOLLICULAR (PREOVULATORY) OVARIAN PHASE
Birth
2 million oocyte s
Puberty
400,000 follicles
Rate of depletion of follicle per month until 35 years old
1000 follicles/month
# of follicles ovulated during the entire reproductive age
400 follicles
percentage of follicles which underwent atresia during lifetime
99.9 %
granulosa cell capacity to convert androstenedione to estradiol is controlled by follicle-stimulating hormone (FSH). After ovulation (right panel), the corpus luteum forms and both theca-lutein and granulosa-lutein cells respond to LH. The theca-lutein cells continue to produce androstenedione, whereas granulosa-lutein cells greatly increase their capacity to produce progesterone and to convert androstenedione to estradiol. LH and hCG bind to the same LH-hCG receptor. If pregnancy occurs (right panel), human chorionic gonadotropin (hCG) rescues the corpus luteum through their shared LH-hCG receptor. Low-density lipoprotein (LDL) is an important source of cholesterol for steroidogenesis. cAMP = cyclic adenosine monophosphate. STAGES OF HUMAN FOLLICULAR DEVELOPMENT EARLY FOLLICULAR PHASE: Inhibin B( granulosa cells) inhibit FSH maturity
Estrogen Surge LH Surge
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only 1 follicle to reach
34 – 36 hours before ovulation precise predictor of ovulation 10 – 12 hours before ovulation
Gonadotropin control of the ovarian and endometrial cycles. The ovarian-endometrial cycle has been structured as a 28day cycle. The follicular phase (days 1 to 14) is characterized by rising estrogen levels, endometrial thickening, and selection of the dominant ―ovulatory‖ follicle. During the luteal phase (days 14 to 21), the corpus luteum (CL) produces estrogen and progesterone, which prepare the endometrium for implantation. If implantation occurs, the developing blastocyst begins to produce human chorionic gonadotropin (hCG) and rescues the corpus luteum, thus maintaining progesterone production. FSH = follicle-stimulating hormone; LH = luteinizing hormone.
FOLLICULAR PHASE
Luteal (Postovulatory) Phase Corpus luteum maintained by LH Estrogen secondary RISE at midluteal phase Progesterone peaks in the midluteal phase
The two-cell, two-gonadotropin principle of ovarian steroid hormone production. During the follicular phase (left panel), luteinizing hormone (LH) controls theca cell production of androstenedione, which diffuses into the adjacent granulosa cells and acts as precursor for estradiol biosynthesis. The
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Human Corpus Luteum Regresses 9 – 11 days after ovulation DECREASED estradiol and progesterone MENSTRUATION WHAT WILL MAINTAIN THE CORPUS LUTEUM HCG IN CASE OF PREGNANCY PROLIFERATIVE PHASE EARLY PROLIFERATIVE PHASE: THIN ENDOMETRIUM Narrow and tubular glands,with Mitotic figures NO extravascular blood or leukocyte infiltration
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Stroma becomes edematous. predecidual transformation of extensive coiling and secretions of glands
PREMENSTRUAL PHASE PREMENSTRUAL PHASE Infiltration of the stroma by polymorphonuclear leukocytes pseudoinflammatory appearance to the tissue MENSTRUAL PHASE SEVERE coiling of the spiral arteries hypoxia of the endometrium stasis/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 ischemiaDYSMENORRHEA DECIDUAL STRUCTURES
Decidua Basalis LATE PROLIFERATIVE PHASE: Endometrium thickens, glandular hyperplasia increase in stromal ground substance (edema and proteinaceous material).
beneath blastocyst implantation
Decidua Capsularis
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Decidua Parietalis
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Overlying the enlarging blastocyst CHORION LAEVE- Internally, avascular extraembryonic fetal membrane Remainder of uterus Fused with capsularis(14-16 weeks) DECIDUA VERA
3 LAYERS OF DECIDUA PARIETALIS AND BASALIS 3 layers 1. zona compacta 2. zona spongiosa 3. zona basalis
zona functionalis
gives rise to new endometrium after delivery
DECIDUAL HISTOLOGY NITABUCH LAYER-zone of fibroid degeneration if defective – Placenta accreta ◦
SECRETORY PHASE EARLY SECRETORY PHASE:
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DATING OF endometrium POSSIBLE glandular epithelium
histology of the
FIRST SIGN OF OVULATION Glycogen accumulates SUBNUCLEAR VACUOLES
Role & Relationship of the Placenta The blood of the mother and baby DOES NOT mix in a HEMOCHORIAL placenta MATERNAL BLOOD IN THE INTERVILLOUS SPACE BATHE THE SYNCITIOTROPHOBLAST BEFORE IT ENTERS THE ENDOTHELIAL WALL OF THE FETAL CAPILLARIES Blastocyst Implantation 6 – 7 days after fertilization STAGE AT THE TIME OF I MPLANTATION
Trophoblast Differentiation Villous trophoblast Extravillous trophoblast intervillous trophoblast endovascular trophoblast Penetrates the spiral artery lumen .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 s trength IN CASE OF INFECTION MAY WEAKENED PROM preterm delivery Amniotic Fluid AF INCREASE UP TO 34 WEEKS then it declines 1,000 ml. at term PHYSIO OB REVIEW FEU-NRMF
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STEROIDOGENESIS Syncitiotrophoblast – major site of steroid production
STEROIDOGENESIS IN PREGNANCY Fetal adrenal secretion of C-19 steroids, precursor of estrogen synthesis LDL-cholesterol from maternal plasma for progesterone biosynthesis HUMAN CHORIONIC GONADOTROPIN (hCG) Alpha sub unit is similar to FSH,LH,TSH Detected in blood and urine either in pregnancy or in neoplastic disease Early pregnancy produced by syncitiotrophoblast and cytotrophoblast
Amniotic fluid
estrogen
Ferning pattern
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OVARIES
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CORPUS LUTEUM functions maximally 6-7 weeks CLINICAL SIGNIFICANCE:DON’T REMOVE ASYMPTOMATIC OVARIAN TUMORS AT THIS TIMEABORTION
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Concentration of hCG in Serum and Urine Detectable in plasma 7 to 9 days after the midcycle LH surge Doubling TIME every 2 days Maximal levels 8 to 10 weeks’ gestation 60th and 80th days after the last menses - peak levels 100,000 mIU/mL •
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Significance of Abnormally High or Low hCG levels HIGH hCG LEVELS Multifetal pregnancy Erythroblastosis fetalis (Fetal hemolytic anemia) Gestational Trophoblastic Disease Fetus w/ Down Syndrome LOW hCG LEVELS Early pregnancy wastage Ectopic Pregnancy •
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THECA-LUTEIN CYST DUE TO HIGH HCG (hyperreactio luteinalis) BILATERAL ASSOCIATED WITH 1. Gestational trophoblastic diseases 2. DM, 3. D-isoimmunization, 4. multiple fetuses 5. chronic renal failure 6. hyperthyroidism Maternal virilization-30% Diagnosis: Ultrasound of enlarged ovaries with multiple cysts Management: self limited; Asymptomatic - resolves after delivery Some – hemorrhage into cysts causing abdominal pain
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Human Placental Lactogen (hPL) Also called human chorionic s omatomammotropin or chorionic growth hormone potent lactogenic and growth hormone-like bioactivity Metabolic Actions of hPL Maternal lipolysis and increase in the levels of circulating free fatty acids Anti-insulin or "diabetogenic" action Potent angiogenic hormone
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PREGNANCY LUTEOMA solid ovarian tumor maternal virilization, but usually female fetus is NOT affected!!! WHY?BECAUSE OF THE CAPACITY OF THE PLACENTA TO CONVERT ANDROGEN TO ESTROGEN Trophoblasts has the capacity to convert androgen and androgen-like factors to estrogen
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Relaxin •
myometrial smooth muscle to promote uterine relaxation and the quiescence observed in early pregnancy
CARBOHYDRATE METABOLISM NORMAL PREGNANCY: Mild fasting hypoglycemia Postprandial hyperglycemia Hyperinsulinemia
POST-PRANDIAL HYPERGLYCEMIA IS DUE TO INCREASED PERIPHERAL INSULIN RESISTANCE TO ENSURE SUSTAINED POST-PRANDIAL GLUCOSE SUPPLY TO THE FETUS
Leptin •
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secreted by adipocytes an anti-obesity hormone - food intake regulates bone growth and immune function correlated positively with fetal birthweight fetal development and growth •
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PREGNANT UTERUS
INSULIN SENSITIVITY is LOWER in pregnancy to about 45-70 % Mediated by: Estrogen and Progesterone Human Placental Lactogen
UTERINE ENLARGEMENT: Stretching and hypertrophy of muscle cells ◦ not hyperplasia INCREASE Fibrous tissue AND elastic tissue ◦
CONTRACTILITY Braxton Hicks irregular, painlesss contractions Unpredictable, sporadic, non-rhythmic, and intensity 5-25 mmHg
FAT METABOLISM MATERNAL HYPERLIPIDEMIA Increase: lipids, lipoproteins, apolipoproteins *Fat is deposited mostly in the central rather than peripheral sites. HEMATOLOGICAL CHANGES IN PREGNANCY HYPERVOLEMIA metabolic demands ◦ support the growing placenta & fetus ◦ protect FROM blood loss ◦ HYPERVOLEMIA after 32-34 week
CERVIX SOFTENING OF CERVIX(GOODELS SIGN) ISTHMUS(HEGARS SIGN) CYANOSIS Cervical Eversion
B ea di ng p at tern
p rog es ter on e
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Mucus plug (Normal)
HGB: will average 12.5 at term Iron requuirement is not available from Marernal storage in most women OPTIMAL INCREASE in maternal erythrocyte VOLUME WILL NOT DEVELOP WITHOUT IRON SUPPLEMENTATION WITH MATERNAL ANEMIA, FETAL RBC PRODUCTION IS NOT INHIBITED
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ACID BASE EQUILIBRIUM Hyperventilationdecreased maternal PCO 2 transport of carbon dioxide from the fetus to the mother and facilitates release of oxygen from maternal blood to the fetus.
DEFINITIONS
URINALYSIS in PREGNANCY Glucosuria may not be abnormal, and is common. Proteinuria is abnormal. Hematuria is usually a result of contamination. URETERAL DILATATION which is greater on the Right side; likely Progesterone effect
NORMAL PREGNANCY DURATION GASTROINTESTINAL TRACT Prolonged gastric emptying time constipation 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, 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
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COMMON CONCERNS
This is just a diagram showing you the weeks of development and wPreimplantation period: 2 weeks from implantation to fertlization Embryonic Period Fetal Period
TERATOGEN Teratogen: may be defined as any agent that acts du ring embryonic or fetal development to produce a permanent alteration of form or function. form and function, acts during embryonic and fetal development most major structural anomalies are easily recognized at birth, and an association with a specific prenatal exposure is likely to be suspected Many congenital abnormalities, however, do not become a pparent until later
STRUCTURAL abnormalities
Food and Drug Administration Categories for Drugs and Medications Category A: Studies in pregnant women have not shown an ◦ increased risk for fetal abnormalities. Examples :Levothyroxine, Potassium ◦ supplementation, and Prenatal multivitamins , when taken at recommended doses. Category B: Animal studies have shown an adverse effect, but ◦ adequate and well controlled studies in pregnant women have failed to demonstrate a risk to the fetus Examples include many antibiotics, such as ◦ penicillins, macrolides, and most cephalosporins Category C: Animal reproduction studies have shown that this ◦ medication is teratogenic (Or embryocidal or has other adverse effect), and there are no adequate and well controlled studies in pregnant women. Approximately two thirds of all medications are in this ◦ category. Category D: This medication can cause fetal harm when ◦ administered to a pregnant woman. systemic cortocosteroids, azathioprine, Phenytoin, ◦ Carbamazepine, Valproic acid, and Lithium. Category X: This medication is contraindicated in women who ◦ are or may become pregnant. May cause fetal harm. ◦ EXAMPLE: rubella vaccine. ◦
HADEGEN AFFECTS THE FUNCTION of an organ TROPHOGEN an agent that alters GROWTH Hadegens and trophogens generally affect processes occurring after organogenesis or even after birth Chemical or physical exposures that act as hadegens or trophogens are much harder to document For simplification, most use the word teratogen to refer to all three types of agents
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Features of Fetal Alcohol Syndrome Minimum amount of alcohol to produce adverse fetal consequences is UNKNOWN. BINGE drinking- high risk for birth defects and increased risk for stillbirth Dose Effect Fetal vulnerability to alcohol is modified by genetic factors, nutritional status, environmental factors, coexisting maternal disease, and maternal age (Abel, 1995). The minimum amount of alcohol required to produce adverse fetal consequences is unknown. Binge drinking, however, 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, 2012; Maier, 2001; Strandberg-Larsen, 2008). ACE Inhibitors and ARBs Enalapril, captopril, lisinopril prolonged fetal hypotension and hypoperfusionrenal ischemia, renal tubular dysgenesis, anuria oligohydramnios lungs & limbs Disrupt the Fetal Renin-Angiotensin system that is essentail in normal Renal development Page 9
Study in 2006: major congenital anomalies: cardiovascular & CNS Angiotensin-converting enzyme (ACE) inhibitors are considered fetotoxic and result in ACE-inhibitor fetopathy. Normal renal development depends on the fetal renal-angiotensin system. ACE-inhibitor medication causes fetal hypotension and renal hypoperfusion, with subsequent ischemia and anuria Reduced perfusion may cause fetal-growth restriction and calvarium maldevelopment, whereas oligohydramnios may result in pulmonary hypoplasia and limb contractures Because angiotensin-receptor blockers have a similar mechanism of action, concerns regarding fetotoxicity have been generalized to include this entire medication class. The possible embryotoxicity of these two drug classes is less certain. First-trimester ACE-inhibitor exposure was associated with a two- to threefold increased risk for cardiac and central nervous system abnormalities, but these observations have not been corroborated. It is reasonable to offer specialized sonography for pregnancies with firsttrimester exposure. Given the many therapeutic options for treating hypertension during pregnancy, it is recommended that ACE inhibitors and angiotensin receptorblocking drugs be avoided.
ANTIFUNGALS Fluconazole Antley Bixler syndrome oral clefts, abnormal facies, and cardiac, skull, long◦ bone, and joint abnormalities 3 fold increase for tetralogy of Fallot ◦ Category D ◦
Sex Hormones Testosterone and Anabolic Steroids virilization and may result in ambiguous genitalia Diethylstilbestrol vaginal and cervical intraepithelial neoplasia Genital tract abnormalities earlier menopause and breast cancer Danazol
MERCURY not a drug, but is a known teratogen developmental delay and mild neurological abnormalities to microcephaly and severe brain damage May be concentrated in large fishes Tuna King mackerel Tile fish FDA recommendation: DO NOT EAT: shark, swordfish, king mackerel & tilefish and more than 6 oz of tuna
RETINOIDS Vitamin A
ANTIMICROBIALS Aminoglycosides gentamicin or streptomycin nephrotoxicity and ototoxicity Medications used to treat infections are among those most commonly administered during pregnancy. Over the years, experience has accrued regarding their general safety. With a few exceptions cited below, most of the commonly used antimicrobial agents are considered safe for the embryo/fetus. Aminoglycosides Preterm infants treated with gentamicin or s treptomycin have developed nephrotoxicity and ototoxicity. Despite theoretical concern for potential fetal toxicity, no adverse effects have been demonstrated, and no congenital defects resulting from prenatal exposure have been identified.
vitamin A supplements may be safe during pregnancy Doses higher than the recommended daily allowance of 5000 IU should be avoided
Isotretinoin
Anti-inflammatory Agents (NSAIDS) Indomethacin and other PG inhibitors 1. Constriction of fetal ductus arteriosus 2. persistent fetal cir culation 3. pulmonary hypertension in the neonate Complications morelikely if the drug is taken >72 hours Importantly, NSAIDs may cause adverse fetal effects when taken in late pregnancy Indomethacin may cause constriction of the fetal ductus arteriosus, resulting in pulmonary hypertension. The drug may also decrease fetal urine production and thereby reduce amnionic fluid volume. This is presumed due to an increase in vasopressin levels and vasopressin responsiveness Fetal ductal constriction is more likely when the drug is taken in the third trimester for longer than 72 hours’ duration. Fortunately, ductal flow velocity returned to normal in all fetuses following discontinuation of therapy. Other NSAIDs are assumed to confer similar risks.
virilization
anti-acne medication ONE OF THE MOST POTENT TERATOGEN IN COMMON USE SIMILAR TO THALIDOMIDE
THALIDOMIDE
Limb-reduction defects (es.upper limbs) Days 27 to 30: upper limb phocomelia Days 30 to 33: lower limb phocomelia GESTATIONAL AGE OR MENSTRUAL AGE time elapsed since the first day of the last menstrual period 280 days or 40 weeks or 9 1/3 calendar months duration
12 Gestational Weeks centers of ossification external genitalia are beginning to show definitive signs of male or female gender 16 Gestational Weeks gender can be correctly determined by experienced observers by inspection of the external genitalia 20 Gestational Weeks Cochlear function - 22 and 25WEEKS 28 Gestatational weeks 90% chance of survival without physical or neurological impairment.
FETAL HEAD Frontal - between the two frontal bones Sagittal - between the two parietal bones Coronal - between the frontal and parietal bones Lambdoid - between the posterior margins of the parietal bones and upper margin of the occipital bone
Chloramphenicol Gray baby syndrome in preterm neonates abdominal distention, ◦ respiratory abnormalities, ◦ an ashen-gray color ◦ vascular collapse ◦ Nitrofurantoin Hyperbilirubinemi a in G6PD deficiency Sulfonamides - Hyperbilirubinemia of a preterm infant Tetracyclines yellowish brown discoloration of deciduous teeth
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Diameters of the head Occipitofrontal (11.5 cm)- root of the nose to the most prominent portion of the occipital bone. Biparietal (9.5 cm) - from one parietal boss to the other. Bitemporal (8.0 cm)- the greatest distance between the two temporal sutures Occipitomental (12.5 cm)- from the chin to the most prominent portion of the occiput. Suboccipitobregmatic (9.5 cm) - from the middle of the large fontanel to the undersurface of the occipital bone
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Circumferences of the head Greatest circumference of the head- corresponds to the plane of the occipitofrontal diameter , averages 34.5 cm
Smallest circumference - corresponding to the plane of the suboccipitobregmatic diameter is 32 cm. Glucose, Insulin, and Fetal Macrosomia fetal hyperinsulinemia insulin-like growth factor and fibroblast growth factor
Sexual Differentiation of the Embryo-Fetus Genetic gender — XX or XY — is established at the time of fertilization.
FETAL PHYSIOLOGY Amnionic Fluid early pregnancy ultrafiltrate of maternal plasma. second trimester extracellular fluid that diffuses through the fetal skin(fetal plasma) After 20 weeks amnionic fluid fetal urine.
Function of the amniotic fluid 1. Cushions the fetus - allows musculoskeletal development - protection from trauma 2. Maintains temperature 3. Minimal Nutritive function 4. Presence of growth factors 5. Growth and differentiation of tissues: lungs, GIT
Surfactant Composition Formed by type II Pneumocytes 90% - lipid 50% dipalmitoylphosphatidylcholine (DPPC) – ◦ principal active component(lecithin) 8-15% phosphatidylglycerol (PG)- capable of ◦ reducing surface tension in the alveolus 5% phosphatidyl ethanolamine ◦ 4% phosphatidyl inositol ◦ 10% - protein
Corticosteroids and Fetal Lung Maturation Fetal cortisol is the natural stimulus for lung maturation Glucocorticosteroids (24-34 weeks) ( betamethasone & dexamethasone ) accelerate fetal lung maturity
Meconium dark greenish-black ( biliverdin) normal bowel peristalsis in the mature fetus vagal stimulation. Hypoxia stimulates arginine vasopressin (AVP) CONTRACTION OF smooth muscle of the colon defecation
Fetal Circulation Umbilical veins oxygenated blood Umbilical arteriesunoxygenated blood CRISTA DIVIDENS preferentially shunts the wel l-oxygenated blood through the foramen ovale Circulatory changes at birth hypogastric arteries umbilical ligaments umbilical vein ligamentum teres. ductus venosus ligamentum venosum Fetal Blood Hemopoiesis yolk sac-first trimester liver-mid pregnancy bone marrow-third trimester
Fetal Hemoglobin fetal erythrocytes( hemoglobin F) bind to oxygen more than hemoglobin A because hemoglobin A binds 2,3-diphosphoglycerate (2,3-DPG) which lowers the affinity of hemoglobin A for oxygen . Fetal Coagulation Factors Factors II, VII, IX, X, XI, prekallikrein, protein S, protein C, antithrombin and plasminogen- 50 % of adult levels CLINICAL APPLICATION: Vit. K is routinely given to newborn after delivery Immunoglobulin G Transfer of IgG from the mother PREVENT INFECTION IN NEONATES BUT CAN BE HARMFUL IN CASE OF: Ex. Hemolytic Disease of the Newborn (resulting from D-antigen alloimmunization) Immunoglobulin M IgM is increased in newborns with congenital infection such as rubella, cytomegalovirus, or toxoplasmosis
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Gonadal Gender If Y chromosome is present(6 weeks )after conception TESTES Phenotypic Gender WITH TESTES male phenotypic sexual differentiation WITHOUT TESTES female differentiation ensues irrespective of the genetic gender.
Fetal Testicular Contributions to Male Sexual Differentiation Müllerian-inhibiting substance
prevents the development of uterus, fallopian tube, and upper vagina Testosterone virilization of the external and internal genital anlagen.
Genital Ambiguity of the Newborn Excessive androgen action in female fetus , or inadequate androgen in one destined to be male. Rarely, genital ambiguity indicates true hermaphroditism. Category 1. Female Pseudohermaphroditism 1. Müllerian-inhibiting substance is NOT produced. 2. Androgen exposure of the embryo-fetus is excessive 3. The karyotype is 46,XX. 4. Ovaries are present. MOST COMMON CAUSE :congenital adrenal hyperplasia Category 2. Male Pseudohermaphroditism Production of müllerian-inhibiting s ubstance. Incomplete but variable androgenic representation for a fetus predestined to be male. A 46,XY karyotype. The presence of testes or no gonads. MOST COMMON CAUSE:ANDROGEN INSENSITIVITY SYNDROME OR REINFENSTEIN SYNDROME Category 3: Dysgenetic Gonads Müllerian-inhibiting substance is NOT produced.
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Fetal androgen exposure is variable. The karyotype varies among subjects and is commonly abnormal. Neither normal ovaries nor testes are present MOST COMMON CAUSE :TURNERS SYNDROME(46X) PHENOTYPICALLY FEMALE WITH SEXUAL INFANTILISM
Category 4: True Hermaphroditism both ovarian and testicular tissues,
Sleep – Awake Cycles Independent of the maternal sleep-awake state Sleep cyclicity - 20 minutes -75 minutes Fetal movement counting Best practice recommendations ACOG (2002): Daily fetal movement count after 28 ◦ weeks' gestation. Perception of 10 distinct movements in 2 hours is ◦ considered reassuring.
Non Stress Test (NST) Test of fetal condition INTERPRETATION: Reactive NST-at least 2 accelerations of 15 beats per min lasting for 15 secs in a 20 min observation INTERVAL OF TESTING:7 DAYS UNLESS HIGH RISK
PRINCIPLE OF NONSTRESS TESTING NON REACTIVE NST: 1. hypoxia 2. neurologic depression 3. fetal sleep 4. medications (magnesium sulfate) 5. maternal cigarette smoking) DECELERATIONS DURING NON STRESS TESTING Repetitive variable decelerations do an ultrasound to check for the amount of amniotic fluid v olume ACOUSTIC STIMULATION TESTS Loud external sounds used to startle the fetus acceleration of the heart rate Positive response fetal heart accelerations following acoustic stimulation
EFM Definition of Terms: Baseline fetal heart rate Heart rate during a 10min segment rounded to the nearest 5bpm increment
Contraction stress test Test of uteroplacental function Fetal heart rate characteristics in response to uterine contractions
Early deceleration EARLY DECELERATION Visually apparent usually symmetrical gradual decrease and return of the FHR to baseline associated with a uterine contraction. 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, 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.
Acceleration
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Late deceleration symmetrical gradual decrease and return of the FHR to the baseline associated with a uterine contraction. The nadir of the deceleration occurs after the peak of the contraction. Significance: UTEROPLACENTAL INSUFFICIENCY
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Interpretation of CST SIGNIFICANCE OF AMNIONIC FLUID VOLUME NORMAL VALUE AFI ( 5 – 24 cm) deepest vertical pocket ( 2- 8 cm)
Sonographic assessment FETAL BIOMETRY monitor lag of growth or absence of growth BIOPHYSICAL SCORE monitor amniotic fluid and fetal behavior DOPPLER VELOCIMETRY assess the adequacy of blood flow in maternal and fetal vessels THE BIOPHYSICAL PROFILE The combined use of 5 fetal biophysical variables is a more accurate means of assessing fetal health than a single element. 5 biophysical components (1) fetal heart rate acceleration (NST) (2) fetal breathing (3) fetal movements (4) fetal tone (5) amnionic fluid volume o
2-5: ULTRASOUND
Significance of AFI < 5 cm: - increased risk of fetal distress - low 5 minute apgar score - 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
FETAL VESSELS: to determine fetal health and for timely delivery of growth restricted fetuses MATERNA VESSELS: to predict placental dysfunction CURRENT ANTENATAL TESTING RECOMMENDATIONS There is no "best test" to evaluate fetal well-being (ACOG,1999) Three testing systems — contraction stress test, nonstress test, and biophysical profile Definitions of the FHR patterns BASELINE Bradycardia Tachycardia
NORMAL: 110-160 bpm <110bpm >160bpm
A BALANCE between sympathetic & paraS (vagal ) stimulation Under the influence of ARTERIAL CHEMORECEPTORS- hypoxia & hypercapnia modulate rate 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 MINIMAL MODERATE MARKED
Amplitude range undetectable Amplitude range 5bpm or fewer Amplitude range of 6-25bpm Amplitude range >25bpm
NST may be omitted if the 4 ultrasound parameters are all normal
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Significance of a normal FHR variability Excellent indicator of good fetal well being INCREASED VARIABILITY WITH fetal breathing, movement, AOG Causes of Decreased or Absent Variability Fetal acidemia, Maternal acidemia Fetal sleep Prematurity Drugs (MgSO4, diazepam, meperidine Vagal blockade (atropine) Defective cardiac conduction system
Reduced baseline heart rate variability is the SINGLE MOST RELIABLE SIGN OF FETAL COMPROMISE
Definitions of the FHR patterns SINUSOIDAL FETAL HEART RATE PATTERN Observed in fetal anemia: Rh isoimmunization, fetomaternal hemorrhage, twin-twin transfusion, vasa previa bleeding
ACCELERATIONS
Accelerations are always reassuring and always confirm that the fetus is not acidemic at that time
Smooth, sine wave like undulating Frequency 2-5/minute for ≥ 20 mins Usually assoc with FETAL ANEMIA Fetal asphxia; chorioamnionitis, fetal distress, cord occlusions Insignificant sinusoidal patterns: meperidine, morphine, butophanol
Visually apparent increase in FHR ≥ 15bpm above baseline lasting ≥ 15 seconds Absence of acceleration is not necessarily an unfavorable sign
PROLONGED deceleration
Isolated decrease in FHR ≥ 15 bpm, ≥ 2 minutes but < 10 mins in duration from onset to return to baseline
Causes of Prolonged Deceleration Common causes Cervical examination Uterine hyperactivity Cord entanglement Maternal supine hypotension Other causes: Conduction analgesia Maternal hypothermia Abruption Umbilical cord prolapse Maternal seizure Valsalva maneuver
FETAL SCALP BLOOD SAMPLING PROTOCOL TO CONFIRM FETAL DISTRESS: pH > 7.25, observe pH 7.20 - 7.25, repeat within 30 minutes. pH is < 7.20, another scalp blood sample is collected if < 7.20 DELIVER FHR TRACINGS FALL INTO ONE OF THREE CATEGORIES
Category III Category II EARLY Decelerations HEAD COMPRESSION
Nadir of the deceleration occurs at the same time as the peak of contraction.
Category I
LATE decelerations UTEROPLACENTAL INSUFFICIENCY
Onset, nadir and recovery of the deceleration occur after the beginning, peak and end of the contraction, respectively.
VARIABLE decelerations UMBILICAL COMPRESSION
An ABRUPT decrease in the FHR below the baseline Less than 30 seconds from onset to nadir
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Clearly abnormal requiring immediate action
Indeterminate requiring careful evaluation and possible corrective measures
Clearly normal requiring no change in management
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: Bradycardia not accompanied by absent baseline o variability Tachycardia o Baseline FHR variability Absent baseline variability not accompanied by o recurrent decelerations Minimal baseline variability o Marked baseline variability o Accelerations Absence of induced accelerations after fetal o stimulation Periodic or episodic decelerations Recurrent variable decelerations accompanied by o minimal or moderate baseline v ariability Prolonged deceleration 2 minutes but < 10 minutes o Recurrent late decelerations with moderate baseline o variability
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Variable decelerations with other characteristics, such as slow return to baseline, "overshoots," 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 o
Category III - Abnormal Absent FHR variability along with any of the following: Recurrent late decelerations o Recurrent variable decelerations o Bradycardia o Sinusoidal pattern o Associated with abnormal fetal acid-base saturation at the time of observation Maternal O2 Discontinue of labor stimulation Treatment of maternal hypotension Change of maternal position Treatment of tachysystole DELIVER
AMNIOINFUSION INDICATIONS: prolonged variable decelerations. oligohydramnios and with PROM dilute or wash out thick mecon ium. PATTERNS OF UTERINE ACTIVITY: Montevideo units to define uterine activity Total uterine pressure per contractions in a 10 minute observation
New Terminology for Uterine Contractions: Normal Uterine Activity: five or less uterine contractions in 10 minutes Tachysystole: more than 5 contractions in 10 minutes
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ETIOLOGY OF BIRTH DEFECTS MALFORMATION - an intrinsic abnormality "programmed" in development a. Example: Spina bifida DEFORMATION - genetically normal fetus develops abnormally because of mechanical forces imposed by the uterine environment. a. Ex: prolonged oligohydramnios->contractures DISRUPTION a more severe change in form or function a. Ex: amnionic band causing a cephalocele or limbreduction abnormality. MULTIPLE STRUCTURAL OR DEVELOPMENTAL ABNORMALITIES SYNDROME - a cluster of several anomalies or defects that have the same cause Example: Trisomy 18 SEQUENCE - anomalies that all develop s equentially as result of one initial insult Example: Oligohydramnios leading to pulmonary hypoplasia, limb contractures, and facial deformities. ASSOCIATION - particular anomalies occur together frequently but do not seem to be linked etiologically •
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Example: VACTERL association: includes three or more of the following – vertebral defects, anal atresia, cardiac defects, tracheoesophageal fistula, renal anomalies, limb abnormalities
PRENATAL DIAGNOSIS OF NEURAL-TUBE DEFECTS NEURAL TUBE DEFECTS (NTD’S) second most common class of birth defect ◦ Open neural-tube defects include: ◦ Anencephaly Spina bifida Cephalocele Other rare spinal fusion (schisis) abnormalities 95% occur without risk factor or family history ◦
RISK FACTORS for NTD’s 1. Family history 2. environmental agents 3. genetic syndrome or anatomical anomalies associated with NTDs 4. high-risk racial or ethnic group 5. anti-folate receptor antibodies 95% of NTD occur in the absence of risk factors Recurrence risk is approximately 4% if a couple previously has a child with NTD – one etiology is a mutation in the MTHFR gene Environmental exposure: hyperthermia, medications that disturb folic acid metabolism, hyperglycemia from IDDM Many women at increased risk for NTD benefit from taking 4mg of FA daily before conception and through the first trimester. Maternal Serum AFP Screening The American College of Obstetricians and Gynecologists (2003) recommends that ALL PREGNANT WOMEN BE OFFERED SECOND-TRIMESTER MATERNAL SERUM AFP SCREENING 15 - 20 weeks Normal Value: =/< 2-2.5 MoM Abnormal screening test - Genetic Counseling consideration for a Diagnostic test(ULTRASOUND) ◦ Some Conditions Associated with LOW Maternal Serum AFP 1. obesity 2. DM 3. Chromosomal trisomies 4. GTD 5. Fetal death 6. Overestimated gestational age
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DOWN SYNDROME low maternal serum AFP levels at 15 to 20 weeks
FIRST TRIMESTER DOWN SYNDROME SCREENING between 11 and 13 6/7 weeks 1. Maternal serum screening free beta hCG ◦ Pregnancy-associated plasma protein A (PAPP-A) ◦ 2. Sonographic evaluation: Nuchal translucency (NT)
The American College of Obstetricians and Gynecologists (2007b) recommends that when the NUCHAL TRANSLUCENCY MEASUREMENT IS 3.5 MM OR GREATER with a normal fetal karyotype, targeted sonographic examination, fetal echocardiography, or both should be considered.
SECOND TRIMESTER DOWN SYNDROME SCREENING Multiple Maternal Serum Markers c ould reliably differentiate pregnancies affected by trisomy 18 and 21 from unaffected pregnancies Serum markers: Triple Test &Quad Test* AFP Human chorionic gonadotropin (hCG) Unconjugated estriol concentration Dimeric inhibin alpha* •
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Ultrasonographic screening for MINOR ABNORMALITIES Nuchal Translucency (NT) – 1st trimester finding Thickened Nuchal Fold – 2nd trimester finding Absent nasal bone Space between the 1st and 2nd toes – Sandal gap AMNIOCENTESIS
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15 and 20 weeks Complications: transient vaginal spotting or amnionic fluid leakage and chorioamnionitis
Femur length (FL) - variation of 7 to 11 days in the second trimester Abdominal circumference (AC) - fetal growth
EARLY AMNIOCENTESIS Between 11 and 14 weeks Same technique Many centers no longer perform amniocentesis before 14 weeks •
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CHORIONIC VILLUS SAMPLING 10 to 13 weeks transcervically or transabdominally, Complications are similar to those of amniocentesis •
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First Trimester ULTRASOUND 1. viability 2. anembryonic gestation / embryonic demise 3.Multifetal gestation - OPTIMAL TIME to determine chorionicity 4.BEST TIME to evaluate the uterus, adnexal structures, and culde-sac Transabdominal scanning Gestational sac – 6 weeks Fetal echoes & cardiac ac tivity – 7 weeks Transvaginal examination Cardiac motion – embryo is 5 mm in length
(CRL= 6wks)
Abdominal Wall Defects Gastroschisis full-thickness defect right of the umbilical cord insertion bowel herniates into the amnionic cavity survival rate 90 percent Cause: early vascular occlusion abdominal wall ischemia. Omphalocele abdominal contents covered only by a two-layered sac of amnion and peritoneum. The umbilical cord inserts into the apex of the sac part of a genetic syndrome, such as Beckwith – Wiedemann or pentalogy of Cantrell Renal Agenesis compressed face, and death from cord compression or pulmonary hypoplasia. renal agenesis Potter syndrome, oligohydramnios sequence. DOPPLER VELOCIMETRY Diminished blood flow may be reflected such a s the following: 1. Diastolic notch 2. Increased SD ratio (Stuart Index) 3. Pulsatility index; Resistance index 4. Absence or reversed end diastolic (ARED) blood flow PELVIC ANATOMY
Fetal Measurements Gestational sac (GS) - 4 – 6 weeks Crown-Rump Length(CRL) - 8-10 weeks Biparietal Diameter (BPD) - 14- 26 weeks most accurate parameter
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LINEA TERMINALIS separates the true and false pelvis
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ISCHIAL SPINES distance between them usually represents the shortest diameter of the pelvic cavity valuable landmarks for fetal head de scent 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
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A, Anteroposterior Diameter 1. Obstetrical conjugate (OC) midposition of the symphysis pubis to pr omontory of ◦ the sacrum
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MIDPELVIS (Plane of least pelvic dimension) Boundaries: Anterior - inferior portion of symphysis pubis Lateral - Ischial spines Posterior – tip of sacrum (1) AnteroPosterior diameter (APM) = 11.5 cm from symphysis pubis to tip of sacrum(4 to 5 th sacral vertebrae) (2) Interspinous diameter (IS)= 10 cm between 2 ischial spines Smallest pelvic diameter (3) Posterior sagittal diameter of the midplane (PSM) = 4.5 cm between sacrum and the line created by the interspinous diameter •
shortest anteroposterior diameter of the inlet Measures >/=10 cm OC= Diagonal conjugate – 1.5-2 cm
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PELVIC OUTLET
2. Diagonal conjugate (DC) lower margin of the symphysis to the promontory of ◦ the sacrum N.V. = 12 cm ◦ 3. True conjugate (TC) ◦ Superior portion of symphysis pubis to promontory of ◦ the sacrum N.V. = 11 cm ◦ TC= Diagonal conjugate-1.2cm ◦
B. Transverse diameter greatest transverse diameter (GTI) - distance between the ◦ linea terminalis = 13.5 cm ◦
Boundaries: Anterior: undersurface of Pubic Arch Posterior - tip of the Sacrum Lateral: Sacrosciatic ligaments & the Ischial tuberosities Anteroposterior diameter of the outlet (APO) – undersurface of pubic arch to tip of the sacrum AP: 9.5-11.5 cm Intertuberous diameter (IT) - between 2 ischial tuberosities IT – 11 cm Posterior sagittal diameter of the outlet* (PSO) – between the tip of the sacrum and the line created by the intertuberous diameter PS: =/> 7.5 cm
PELVIC SHAPES Caldwell and Moloy classification Posterior segment determines the type of p elvis Anterior segment determines the tendency Many pelvis are not pure but are mixed PHYSIO OB REVIEW FEU-NRMF
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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
Android
oval anteroposteriorly > AP diameter than Transverse diameter
poor prognosis for vaginal delivery
Platypelloid Short AP and wide Transverse diameters
Phase 1 of Parturition: Uterine Quiescence and Cervical Softening Uterine Quiescence Braxton Hicks contractions or False labor ◦ 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, described ◦ by women as ―THE BABY DROPPED.‖ Phase 3 of Parturition: Labor Stages of Labor First stage ◦ Stage of cervical effacement and dilatation Ends when the cervix is fully dilated( 10 cm) The Second stage ◦ Stage of fetal expulsion Begins when cervical dilatation is complete(10cms) and ends with delivery Third stage of labor ◦ Stage of placental separation and expulsion Begins after delivery of the fetus and ends with the delivery of the placenta 2 Phases of cervical dilatation: Latent phase ◦ variable and sensitive to extraneous factors , sedation and myometrial stimulation Active phase ◦ Acceleration phase predictive of the outcome of a particular labor
Engagement Descent of the biparietal plane of the fetal head to a level below that of the p elvic inlet IF HEAD is engaged the INLET is adequate ascertained by vaginal exam and by abdominal palpation When the lowermost portion of the fetal head is at or below the ischial spines, it is usually engaged EXCEPT if there is molding or caput formation PELVIC OUTLET MEASUREMENTS Intertuberous diameter (IT) = >8cm Distance between two ischial tuberosities Place a closed fist against the perineum between two ischial tuberosities Midpelvis Estimation Suspicious findings for MIDPELVIC CONTRACTION Prominent ischial spines sidewalls are convergent shallow concavity of the sacrum PHYSIO OB REVIEW FEU-NRMF
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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.‖ ◦ Causes of labor pains: (1) hypoxia of the contracted myometrium (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)
As labor progresses, sinciput and brow presentations almost always convert into vertex or face presentations by neck flexion or extension, respectively.
Distinct Lower and Upper Uterine Segments
UPPER SEGMENT: firm during contractions contracts,retracts and expels fe tus LOWER SEGMENT: Softer ,distended and more passive
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
BREECH PRESENTATION Frank Breech – thighs are flexed and the legs extended Complete Breech – thighs AND legs are flexed Incomplete, or Footling Breech - if one or both feet, or one or both knees, are lowermost or extended
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: SCHULTZE Central separation, 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
FETAL POSITION relationship of the chosen portion of the fetal presenting part to the right or left side of the birth canal.
Phase 4 of Parturition: The Puerperium lactogenesis and milk let-down Reinstitution of ovulation Within 4 to 6 weeks after birth, 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, placenta previa, › hydramnios, and uterine anomalies Oblique Lie 45-degree angle › unstable ›
FETAL ATTITUDE UNIVERSAL FLEXION the arms are usually crossed over the thorax or become parallel to the sides. The umbilical cord lies in the space between them and the lower extremities. FETAL PRESENTATION portion of the fetal body foremost within the birth canal
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Varieties of Presentations and Positions Shoulder presentations( acromion (scapula) is the portion of the fetus Another term used is transverse lie, with back up or back down.
DIAGNOSIS OF FETAL PRESENTATION AND POSITION LEOPOLD’S MANEUVER L1, L2 and L3 – examiner stands at the side of the bed and faces the patient L4 – examiner faces patients feet
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First Maneuver – Fundal Grip Breech – sensation of a large, nodular body Cephalic – hard and round movable and balottable Second Maneuver – Lumbar Grip Back – hard, resistant Extremities – numerous small, irregular and mobile parts Third Maneuver – Pawlik’s grip The lower portion of the abdomen is grasped just above the symphysis pubis Engaged or not engaged
Extension
External Rotation bisacromial diameter into relation with the anteroposterior diameter of the pelvic outlet Expulsion
Fourth Maneuver – Pelvic grip DETERMINE THE CEPHALIC PROMINENCE Vertex Presentation – the prominence is on the same side as the small parts Face Presentations – the prominence is on the same side as the back
anterior shoulder appears under the s ymphysis pubis. After delivery of the shoulders, the rest of the body quickly passes.
ASYNCLITISM It is the lateral deflection of the head to a more anterior or posterior position in the pelvis
CARDINAL MOVEMENTS OF LABOR 1. Engagement 2. Descent 3. Flexion 4. Internal Rotation 5. Extension 6. External Rotation 7. Expulsion
Head presses upon the pelvic floor Two forces : 1. exerted by the uterus 2. resistant pelvic floor
1. 2.
2 TYPES OF ASYNCLITISM ANTERIOR ASYNCLITISM POSTERIOR ASYNCLITISM
ANTERIOR ASYNCLITISM Sagittal suture approaches the sacral promontory o More of the ANTERIOR parietal bone pr esents o
POSTERIOR ASYNCLITISM Sagittal suture lies close to the symphysis o POSTERIOR parietal bone will present o 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. The latent phase for most women ends at between 3 and 5 cm of dilatation.
CARDINAL MOVEMENTS OF LABOR Descent first requisite for birth of the newborn Nulliparas= engagement before labor, and further descent follow until the onset of the second stage Multiparous= descent begins with engagement
Prolonged Latent Phase > 20 hours in nullipara >14 hours in multipara Active Labor cervical dilatation of 3 to 5 cm or more, in the presence of uterine contractions
Four forces FOR DESCENT 1. pressure of the amnionic fluid 2. direct pressure of the fundus upon the breechs 3. bearing down efforts 4. 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
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ABNORMAL LABOR PATTERNS, DIAGNOSTIC CRITERIA, AND METHODS OF TREATMENT
THIRD STAGE
15-30 mins
15-30 mins
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. Rapid Labor 2. Early detection of meconium staining 3. 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. Calkin’s Sign – the uterus becomes globular The earliest SIGN to appear. 2. Sudden gush of blood 3. Uterus rises in the abdomen 4. 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
DETECTION OF RUPTURED MEMBRANES SIGNIFICANCE 1. prolapse of the umbilical cord 2. labor is likely to occur 3. increased incidence of intrauterine infection
OXYTOCIC AGENTS Oxytocin (pitocin, syntocinon) Not effective by mouth SIDE EFFECTS: ANTIDIURETIC/HYPOTENSION NOT GIVEN AS IV BOLUS
DIAGNOSIS 1. amniotic fluid pooling 2. Testing the pH of the vaginal fluid : pH above 6.5 is consistent with ruptured membranes 3. the use of the indicator Nitrazine yellow-->blue 4. Other Tests : Arborization or ferning pattern alpha-fetoprotein positive injection of various dyes into amniotic sac STATION
When lowermost portion of presenting part is at level of ischial spines designated as zero Divisions represent cms above and below the spines into fifths
DURATION OF STAGES OF LABOR Nullipara
Multipara
Latent Phase
<20 hours
<14 hours
Active Phase
1.2cm/hr
1.5cm/hr
FIRST STAGE
SECOND STAGE
50 mins
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Active management of the 3rd stage UTERINE MASSAGE OXYTOCIN, ERGONOVINE, AND METHYLERGONOVINE
Ergonovine and Methylergonovine From ergot Powerful stimulants of myometrial contraction SIDE EFFECTS: transient severe hypertension NOT USED IN PATIENTS WITH BRONCHIAL ASTHMA Prostaglandins Not used routinely management of postpartum hemorrhage due to uterine atony PG F2-NOT USED IN B. ASTHMA PG E2-SAFE FOR BRONCHIAL ASTHMA LACERATIONS OF THE BIRTH CANAL First Degree Laceration fourchette, perineal skin and vaginal mucous membrane Second Degree Laceration skin and mucous membrane, the fascia and muscles Third Degree Laceration skin, mucous membrane, perineal body and sphincter Fourth Degree Laceration Extends through the rectal mucosa to expose the lumen of the rectum
20 mins
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MIDLINE versus MEDIOLATERAL EPISIOTOMY
LACTATION COLOSTRUM deep lemon-yellow-colored liquid 2nd postpartum day rich in immunological components(Ig A), minerals, amino acid,protein but less sugar and fat
Characteristic
Midline
Mediolateral
Surgical repair
Easy
More difficult
Faulty hearing
Rare
More common
Postoperative pain
Minimal
Common
HUMAN MILK All vitamins EXCEPT VIT K are found in human milk Vitamin K after delivery is required to prevent hemorrhagic disease of the newborn
Anatomical results
Excellent
Occasionally faulty
IMMUNOLOGICAL CONSEQUENCES OF BREASTFEEDING
Blood loss
Less
More
Dyspareunia
Rare
Occasional
Extensions
Common
Uncommon
PUERPERIUM considered to be between 4 and 6 weeks
INVOLUTION OF THE REPRODUCTIVE TRACT UTERINE INVOLUTION 4 weeks after delivery uterus regains its previous nonpregnant size ◦ LOCHIA LOCHIA RUBRA- first few days after delivery, RED color i LOCHIA SEROSA- After 3 or 4 days, PALE in color LOCHIA ALBA- After about the 10th day, WHITE or YELLOWISH WHITE color
DECIDUA AND ENDOMETRIAL REGENERATION Superficial layer BECOMES NECROTIC--> sloughed in the lochia ◦ Basal layer adjacent to the myometrium--> the source of new ◦ endometrium
LACTATION INHIBITION Milk leakage, engorgement, and breast pain ( 3 to 5 days) TREATMENT: Ice packs analgesics Bromocriptine , for lactation inhibition is associated with strokes, myocardial infarctions, seizures, and psychiatric disturbances. CONTRACEPTION FOR BREASTFEEDING WOMEN Recommendations for Hormonal Contraception if Used by Breast Feeding Women 1.Progestin-only oral contraceptives --> started 2 – 3 weeks postpartum 2.Depot medroxyprogesterone acetate --> 6 weeks postpartum.a 3.Hormonal implants -->inserted at 6 weeks postpartum. CONTRAINDICATIONS TO BREASTFEEDING Breastfeeding is not contraindicated if hepatitis B immune globulin is given to infants of seropositive mothers. Hepatitis C infection is not a con traindication to breast feeding Herpes simplex virus if there are no breast lesions is NOT a contraindication to breast feeding
SUBINVOLUTION arrest or retardation of involution Causes: Infection ◦ retained placental fragments ◦ incompletely remodeled uteroplacental arteries ◦ SIGNS AND SYMPTOMS irregular or excessive uterine bleeding ◦ uterus is larger and softer ◦
Management of Subinvolution Ergonovine or methylergonovine ◦ Antibiotic therapy for infection ◦ Chlamydia trachomatis ◦ MOST COMMON CAUSE MANAGEMENT: Azithromycin or Doxycycline
6 weeks
PLACENTAL SITE INVOLUTION ◦
Complete extrusion of the placental site
LATE POSTPARTUM HEMORRHAGE American College of Obstetricians and Gynecologists (2013b) bleeding 24 hours to 12 weeks after delivery ◦ Causes: MOST COMMON CAUSE: ◦ retention of a placental fragments ◦ Treatment oxytocin, ergonovine, methylergonovine, or ◦ prostaglandins Antimicrobial – with infection ◦ Suction curettage – large clots ◦ Curettage- NON RESPONSIVE TO medical ◦ management
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SECRETORY IgA less prone to enteric infection aga inst rotavirus infections,Escherichia coli infections contains both T and B lymphocyte
BREAST FEVER breasts -->distended, firm, and nodular elevation of temperature (ranged from 37.8 to 39°)
Treatment: binder or brassiere, ice bag, analgesic, pumping of the breast
MASTITIS unilateral, marked engorgement, inflammation. chills, fever and tachycardia. ETIOLOGY: Staphylococcus aureus – 40 %; c Immediate source of organisms --> infant's nose and throat
TREATMENT: MASTITIS culture of the expressed milk antimicrobial therapy: Dicloxacillin 500 mg orally four times daily, ◦ Erythromycin if penicillin sensitive ◦ Vancomycin is effective against MRSA ◦ treatment for 10 to 14 days Postpartum blues- degree of depressed mood a few days after delivery Excitement and fears during pregnancy and delivery ◦ Discomforts of the early puerperium ◦ Fatigue from loss of sleep during labor and postpartum ◦ anxiety over the ability to provide appropriate infant care, and ◦ body image concerns TREATMENT anticipation, recognition, and reassurance Mild and self-limited to 2 to 3 days, although it sometimes lasts for up to 10 days
CONTRACEPTION Not breastfeeding, menses usually return within 6 to 8 weeks
HOME CARE COITUS - no definite time after delivery when coitus should be resumed -coitus may be resumed based on the patient's desire and c omfort Page 22
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ANESTHESIA AND ANALGESIA MATERNAL RISK FACTORS THAT SHOULD PROMPT ANESTHESIA CONSULTATION: •
1. Marked Obesity
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2. Severe edema or anatomical abnormalities of face, neck, or spine, including trauma or surgery
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Lidocaine or Chloroprocaine at 3 and 9 o’clock Complication: fetal bradycardia
SPINAL (SUBARACHNOID) BLOCK Vaginal Delivery forceps or vacuum delivery T10 dermatome Lidocaine or Bupivacaine Cesarean Delivery T4 dermatome
3. Abnormal dentition, small mandible, or difficulty opening mouth 4. Extremely short stature , short neck, or arthritis of the neck
COMPLICATIONS OF SPINAL (SUBARACHNOID) BLOCK Hypotension High spinal blockade Spinal (Postural puncture) headache Convulsions Bladder dysfunction Oxytocics and hypertension Arachnoiditis and meningitis •
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5. Goiter
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6. Serious maternal medical problems, such as cardiac, pulmonary or neurological disease
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7. Bleeding disorders 8. Severe preeclampsia 9. Previous history of anesthetic complications
Contraindications to Spinal Anesthesia ABSOLUTE CONTRAINDICATIONS hypotension coagulopathy bacteremia Skin infection Increased intracranial pressure •
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10. Obstetrical complications likely lead to operative delivery – e.g., placenta previa or higher-order multiple gestation
Goals for Optimizing Obstetrical Anesthesia Services Nonpharmacological Methods of Pain Control 1. LAMAZE teaching pregnant women relaxed breathing and their labor partners psychological support techniques. 2. CLINICAL HYPNOSIS – power of the mind to heal the body; increases of beta endorphins in the peripheral blood 3. ACUPUNCTURE •
EFFICACY AND SAFETY OF PARENTERAL AGENTS Meperidine is the most common opioid used worldwide for pain 1. relief in labor. Meperidine or other narcotics – cause newborn respiratory depression •
NARCOTIC ANTAGONISTS Naloxone Reverses respiratory depression induced by opioid narcotics NITROUS OXIDE 50% nitrous oxide and oxygen provides satisfactory analgesia during labor •
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REGIONAL ANALGESIA SENSORY INNERVATION OF THE GENITAL TRACT Uterine Innervation Early in labor – SENSORY T11 and T12 nerves Motor pathways – T7 and T8 vertebrae
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EPIDURAL ANESTHESIA Continuous Lumbar Epidural Block VAGINAL DELIVERY - T10 to S5 CESAREAN DELIVERY - T4 to S1 •
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COMPLICATIONS OF EPIDURAL ANESTHESIA Total spinal blockade Ineffective analgesia Hypotension Central nervous stimulation Maternal pyrexia Back pain •
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Effects on Labor Prolongs active phase of labor by 1 hour Increases the need for instrumental delivery LIKE FORCEPS AND VACUUM due to prolonged second-stage labor •
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Contraindications Hemorrhage •
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ANESTHETIC AGENTS (Table 19-3. Some Local Anesthetic Agents us ed in Obstetrics)
Central Nervous System Toxicity Bizarre behavior, slurred speech, muscle fasciculation and excitation, generalized convulsions, loss of consciousness •
Cardiovascular Toxicity Hypertension , tachycardia, hypotension and cardiac arrhythmias
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PUDENDAL BLOCK Relatively safe and simple Complications: serious systemic toxicity, hematoma formation from perforation of a blood vessel
Suspicion of neurological disease Anticoagulation •
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Lower Genital Tract Innervation Pudendal nerve – sensory nerve fibers from S2 through S4 nerves Passes beneath the posterior surface of the sacrospinous ligament just as the ligament attaches to the ischial spine
Infection at or near the sites of puncture
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Severe Preeclampsia-Eclampsia BEST ANESTHESIA: EPIDURAL ANESTHESIA
GENERAL ANESTHESIA PATIENT PREPARATION ANTACIDS UTERINE DISPLACEMENT Lateral uterine displacement Preoxygenation
Thiopental •
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Ease and rapid/ minimal risk of vomiting Poor analgesic agents May cause newborn depression
Ketamine •
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causes a rise in blood pressure Unpleasant delirium and hallucination.
INTUBATION Sellick maneuver – Cricoid pressure is used to occlude the esophagus from induction until intubation •
Failed Intubation Morbid obesity is also a major risk factor for failed or difficult intubation. •
PARACERVICAL BLOCK Pain relief during the first stage of labor
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GAS ANESTHETICS Volatile Anesthetics Most commonly used is isoflurane. produce remarkable uterine relaxation USES: Internal podalic version of the second twin Breech decomposition Replacement of acutely inverted uterus . ASPIRATION Aspiration pneumonitis has been the most common cause of anesthetic deaths in obstetrics. •
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ASPIRATION Aspiration pneumonitis has been the most common cause of anesthetic deaths in obstetrics. A fasting period of 8 hours or more is preferable for uncomplicated parturients undergoing elective cesarean delivery. FASTING A fasting period of 8 hours or more is preferable for uncomplicated parturients undergoing elective cesarean delivery.
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