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Ma. Bernadette O. Cruz, MD, MSc, FPOGS
Selected maternal and fetal conditions that make the pregnancy at risk for maternal and fetal morbidity and mortality.
Multifetal pregnancy Preterm labor Postterm pregnancy Inappropriate fetal growth Premature rupture of membranes Congenital malformations and inherited diseases Diseases and injuries of the fetus and the newborn infant
VARIATIONS IN THE DURATION OF PREGNANCY
Average duration of normal pregnancy
260 days from conception 280+14 days from LMP
Incidence of preterm birth - 5% of pregnancies (<36 weeks) 10% of cases, the pregnancy is prolonged.
birth >41 weeks
Preterm Labor and Delivery .
Preterm Delivery Preterm – infants delivered before completion of 37 weeks (259th day) Low birthweight – <2500 grams Very low birthweight – <1500 grams Extremely-low birthweight – <1000 grams .
c. e. d. Medical and obstetric complications a. d.Etiology of preterm labor 1. g. f. b. h. f. low prepregnancy weight smoking alcohol abuse Young gravida Poverty short stature occupational factors psychological stress . Preeclampsia fetal distress fetal growth restriction abruptio placentae fetal death spontaneous preterm labor b. 2. Lifestyle factors a. c. e.
4. tumor necrosis factor. Genetic factors Amnionic fluid and chorioamnionic infection initiated by secretory products (interleukin1. interleukin-6) resulting from monocyte activation in response to infection Phospholipase A cleaves arachidonic acid prostaglandin synthesis .Etiology of preterm labor 3.
Multiple gestation – although incidence is only 1. maternal age <18 years or >40 years. . nonwhite race. Epidemiologic studies: Low SES.Etiology of preterm labor 5.1%. MP accounts for 10% of all preterm births 6. low prepregnancy weight.
No PNC regardless of SES 9. 8. Risk of preterm birth increases with women who had spontaneous second-trimester abortion(s).Etiology of preterm labor 7. History of preterm birth Recurrence risk: of 17-37% Risk increases with number of preterm births and decreases with number of term deliveries. .
11. sexual abstinence in the prevention of preterm labor (?). PROM Uterine malformations – unicornuate and bicornuate uteri Uterine myoma – submucosal or subplacental . 13. 12.Etiology of preterm labor 10. Coitus and orgasm (?).
trachomatis. U.1-2% of all pregnancies due to trauma from prior obstetric or gynecologic procedure. Cervical incompetence 0. . vaginalis or G vaginalis. Infectious causes STDs Chorioamnionitis Group B streptococci. C. N. pallidum. diethylstilbestrolexposure in utero 15. gonorrhoeae. urealyticum. T.Etiology of preterm labor 14. T.
pelvic pressure Watery or bloody vaginal discharge Menstrual-like cramps and low back pain Asymptomatic cervical dilatation after midpregnancy mean cervical length (UTZ) at 24 weeks = 35 mm women with progressively shorter cervices experienced increased rates of preterm birth .Signs and symptoms Painful or painless uterine contractions.
fibroblasts. Fetal fibronectin A glycoprotein produced by fetal amnion. hepatocytes. malignant cells.Diagnostics: 1. adhesion of placenta to decidua Detection of fetal fibronectin in cervicovaginal secretions prior to membrane rupture may be a marker for impending preterm labor . endothelial cells Plays a role in intercellular adhesion: implantation.
Diagnostics 2. maternal salivary estriol associated with preterm delivery . Ambulatory uterine contraction testing – use of home monitoring of uterine contractions for prevention of preterm labor controversial 3.
Contractions occurring at a frequency of four in 20 minutes or eight in 60 minutes + progressive change in the cervix 2. Cervical dilatation > 1 cm 3. 1997) CRITERIA FOR DIAGNOSIS 1. Cervical effacement of > 80% .(American Academy of Pediatrics and the American College of Obstetricians and Gynecologists.
Gestational age? Condition of membranes? Successful treatment achieved when initiated early. before advanced cervical dilatation and rupture of membranes .Management 1. 2.
Premature labor with intact membranes Glucocorticoid therapy A.1. Corticosteroids accelerate lung maturation lower incidence of RDS. mortality from hyaline membrane disease Induction of proteins that regulate biochemical systems within type II cells in the fetal lung to produce surfactant B. Cervical cerclage – in recurrent midtrimester losses .
Premature labor with intact membranes C. chlamydial most often used treatment regimen D. Treat bacterial vaginosis linked to increased preterm birth at <32 weeks or less treatment of asymptomatic BV did not improve pregnancy outcomes Other vaginal infections: trichomoniasis. Bed rest no conclusive evidence that bed rest is effective E. Hydration and sedation .
Premature labor with intact membranes F. 4. 3. Tocolysis 1. Beta-adrenergic receptor agonists Magnesium sulfate Prostaglandin inhibitors Calcium channel blockers . 2.
Loss of DTRs at 10 mEqs. Respiratory paralysis at 15 mEqs Cardiac arrest at 25 mEqs Example Ritodrine. capillary permeability. myocardial ischemia Hyporeflexia at 6-12 mEq/L. terbutaline Magnesium sulfate . activates adenylate cyclase. inc. increases cAMP which reduces intracellular calcium Side Effects Pulmo edema. arrhythmia.Tocolytic Agents DRUGS badrenergic receptor agonist Mechanism Combines w/ receptor to activate adenyl cyclase w/c converts ATP to cAMP. decreases intracellular CA+ prevents contraction blocks calcium influx at membrane.
blocks action of PGs on target organs. sulindac Prostaglandin inhibits synthesis inhibitor of PGs. PGs are involved in myometrial contractions of normal labor Calcium channel blockers inhibit entry of CA+ thru cell membrane channels reduction in CA+ concentration inhibits contraction maternal Nifedipine hypotension and decreased uteroplacental perfusion. intracranial hemorrhage Example Indomethacin. necrotizing enterocolitis.Tocolytic Agents DRUGS Mechanism Side Effects closure of ductus arteriosus. tachycardia .
competitive oxytocinvasopressin antagonist potent endogenous smoothmuscle relaxant Side Effects Example Nitric oxide .Tocolytic Agents DRUGS Atosiban Mechanism oxytocin analog.
Preterm labor + preterm premature rupture of membranes (PPROM) Expectant management or nonintervention – spontaneous labor is simply awaited Corticosteroids + tocolytic agents to allow corticosteroids to work (induce fetal lung maturation) .Management 2.
Premature rupture of membranes (PROM) .
Premature rupture of membranes
Rupture of membranes before onset of labor
25% of cases the fetus is preterm.
Preterm premature rupture of membranes – rpture of membranes before onset of labor at gestational age <37 weeks. Prolonged rupture of membranes – PROM >24 hours before delivery. Latency period – time between PROM and onset of labor.
Amniotic fluid is necessary for normal fetal lung development. It also protects the fetus from trauma and umbilical cord from compression. RUPTURE OF MEMBRANES
Premature rupture of membranes
May lead to onset of preterm labor In most cases, the baby is born within 7 days of the prelabor rupture.
Prolonged PROM increases risk for chorioamnionitis.
Local infection – weakening of membranes N. Group B strep. vaginalis 2. 4. 5. C. gonorrhoeae. G. 3. 6. trachomatis. Polyhydramnios Incompetent cervix Cervical cerclage Previous cervical laceration or operation Smoking .Risk factors for PROM 1. T. vaginalis.
excessive vaginal discharge or mucus.Clinical presentation Gush of fluid from the vagina followed by persistent leakage of fluid (90%) Differentiate from urine. bloody show associated with labor Chorioamnionitis Preterm labor .
5 – 6 AF pH: 7.Diagnostics 1.1 – 7.3 Nitrazine paper: yellow blue pH >6. Tests to document rupture of membranes Nitrazine test for pH of vagina Normal vaginal pH: 4.0 Microscopic slide test for ferning of vaginal fluid (+) ferning with AF .
Diagnostics 2. Ultrasound examination Establish AOG Fetal presentation Low AF index 3. Cervical cultures .
c. CBC with differential Serum C-reactive protein >0.8 mg/dl Amniocentesis and AF culture Biophysical profile a.Diagnostics 4. Fetal breathing movements Gross body movement Fetal tone Reactive FHR Qualitattive AFV . b. d. d. e. Tests to rule out chorioamnionitis a. b. c.
c. d. Tests for fetal lung maturity a.Diagnostics 5. b. Fetal lung maturity – impt factor in PROM Lecithin-sphingomyelin (L/S) ratio >2 (+) Phosphatidylglycerol Foam stability test – shake test a. High false-negatives: LS ratio 4-6 . AF with sufficient surfactant forms stable stable foam at air-surface interface for 15 min a.
STD) PROM at term: 90% of patients will go into labor <24 hours PPROM 28-34 weeks AOG: 50% in labor within 24 hours.Complications from PROM Threats to the fetus 1. 80-90% within 1 week PPROM <26 weeks: 50% in labor within 1 week . Prematurity Responsible for 30% of all preterm births (>low SES.
Infection Serous infection: 5% of preterm PROM 15-20% with chorioamnionitis Fetal pneumonia. conjunctivitis Incidence: 8. Fetal distress .5% (6-fold increase in risk) Umbilical cord compression or prolapse 3.Complications from PROM Threats to the fetus 2. UTI. sepsis.
5%) esp <26 weeks AOG .Complications from PROM Threats to the fetus Fetal deformations Early preterm PROM: impaired feltal lung development pulmonary hypoplasia IUGR Compression malformations of face and limbs (3.
Preterm PROM: 15-25% .5-1%.Complications from PROM Threats to the Mother Sepsis secondary to chorioamnionitis Overall: 0. Prolonged PROM chorioamnionitis: 315%.
PROM + advanced labor. fetal distress regardless of gestation Vaginal delivery CS for obstetric reasons Antibiotic treatment Ampicillin Cephalosporins Gentamycin . chorioamnionitis.Management of PROM 1.
b. Expectant management Induction of labor immediately . PROM at term Goal: deliver before chorioamnionitis a.Management of PROM 2.
Management of Term PROM Expectant management a. b. d. e. Await spontaneous labor Avoid digital cervical examination until patient in labor c. Electronic fetal heart monitoring Serial monitoring for chorioamnionitis Deliver ASAP if (+) chorioamnionitis .
Continuous electronic fetal heart monitoring .Management of Term PROM Labor induction immediately a. Induce labor with oxytocin infusion Intracervical prostaglandin E2 gel for preinduction cervical ripening Bishop’s score b.
Expectant management Tocolysis + corticosteroids followed by delivery . 2. prolong pregnancy for as long as no chorioamnionitis 2 Options 1.Management of PRETERM PROM Prematurity if not in labor.
Prophylactic antibiotics Decreases maternal and fetal infections Increases latency period by 5-7 days 2.Management of PRETERM PROM: Expectant management 1. 4. 5. 3. 6. Bed rest Avoid digital cervical exam until labor Fetal well-being studies Serial monitoring for chorioamnionitis Test for fetal lung maturity if >32 weeks .
Expectant management or induce labor . Tocolysis Continued for 48 hrs after steroids 3.Management of PRETERM PROM: Tocolysis + corticosteroids followed by delivery 1. Corticosteroid therapy Maximum effect 24 hours after administration 2.
2. Expectant management Termination of pregnancy .Management of PREVIABLE PROM PROM <25 weeks 25-40% chance of achieving viable fetus Risk of chorioamnionitis: 40% Fetal deformities Counseling for couple 2 Options 1.
MULTIFETAL PREGNANCY .
dizygotic or fraternal twins).ETIOLOGY Monozygotic twins arise from a single fertilized ovum that subsequently divides into two similar structures. Dizygotic twins result from fertilization of two separate ova (double-ovum. . each with potential for developing into a separate individual (single-ovum. monozygotic or identical twins).
1. Dizygotic twins . Monozygotic twins 2.
Chimerism - .in an individual whose cells originated from more than one fertilized ovum. 3.
nor necessarily by sperm from the same male. Superfecundation refers to the fertilization of two ova within a short period of time but not at the same coitus.ETIOLOGY Superfetation when an interval as long as or longer than an ovulatory cycle intervenes between fertilizations. .
ETIOLOGY OF MULTIFETAL PREGNANCY
RISK FACTORS FOR TWINNNG
Heredity – maternal family history > paternal Maternal age – peak at age 37, when maximum hormonal stimulation increases rate of double ovulation
Parity – fertility and multiparity (~7)
RISK FACTORS FOR TWINNNG
Pituitary gonadotropin – common factor linking race, age, weight, and fertility to multiple gestation.
Infertility therapy – induction of ovulation by use of gonadotropins (FSH plus HCG) or clomiphene.
DIAGNOSIS: History and PE 1. Physical examination . History identification of risk factors Fundic height larger than expected for gestational age Multiplicity of fetal parts by palpation Two distinct fetal heart tones 2.
DIAGNOSIS: 3. . Ultrasound Presence of 2 separate placental sites and a thick dividing membrane that generally is 2 mm or greater supports dichorionicity.
DIAGNOSIS: Ultrasound “Twin peak” sign – triangular projection of placental tissue extending beyond the chorionic surface between the layers of the dividing membrane seen in fused placenta .
Biochemical test: Human chorionic gonadotropin in plasma and urine are higher than those in singleton pregnancies Radiograph of the maternal abdomen demonstrates multiple fetuses. .DIAGNOSIS 4. helpful in rare circumstances 5.
> in singleton pregnancy 2.Maternal Adaptations to Multifetal Pregnancy 1. Blood volume expansion 50-60% with twins vs 40-50% with singletons more pronounced “physiologic anemia” . Nausea and vomiting .
Cardiac output – increased due to increased heart rate and stroke volume 4.Maternal Adaptations to Multifetal Pregnancy 3. Uterus – larger size (volume of 10L. weight of 20 lbs) .
Defects from twinning itself Defects from vascular interchange Defects due to crowding . Spontaneous abortion more common in monozygotic twins. Malformations 2.OUTCOMES OF MULTIFETAL PREGNANCY 1.
Defect from twinning: Conjoined twins .
Defect from twinning: SIRENOMELIA Persistence of vitelline artery abnormal aortic development blood flow to lower extremities curtailed .
cleft lip and palate. internal organs .Defect from twinning: Holoprosencephaly Failure of brain to divide into hemispheres. deformities of limb. GIT. Always accompanied by midline defects e.g. fused eye sockets. heart.
Defect from twinning: Neural tube defect .
Defect from twinning: Neural tube defect Exencephaly .
Folic acid in the prevention of NTDs .
Defects from vascular interchange: ACARDIA .b.
Defects from vascular interchange: Microcephaly .
Defects from vascular interchange: INTESTINAL ATRESIA .
Defects from vascular interchange: APLASIA CUTIS .
Defect from crowding: Talipes .c.
OUTCOMES OF MULTIFETAL PREGNANCY Low birthweight From restricted fetal growth and preterm delivery Degree of growth restriction related to monozygosity and number of twins Monozygotic twins more likely to be discordant in size.3. .
.OUTCOMES OF MULTIFETAL PREGNANCY 4. Major reason for the increased risk of neonatal death and morbidity in twins. Preterm birth Duration of gestation decreases as the number of fetuses increases.
Long-term postnatal development twinning may result to delayed developmental milestones. 6. Prolonged pregnancy fetal growth restriction and associated morbidity increases significantly in twins delivered at 39-41 weeks compared with delivery at 38 weeks or less. . pattern of development appears to be better in the twin who weighed more at birth. in discordant twins.OUTCOMES OF MULTIFETAL PREGNANCY 5.
OUTCOMES OF MULTIFETAL PREGNANCY 7. Conjoined twins twinning initiated after the embryonic disc and rudimentary amnionic sac have formed and if the division of the embryonic disc is incomplete commonly shared body site: anterior (thoracopagus) posterior (pyopagus) cephalic (craniopagus) caudal (ischiopagus) .
PYGOPAGUS Conjoined twins THORACOPAGUS CRANIOPAGUS .
vein-to-vein. or artery-tovein . Monoamnionic twins – intertwining of umbilical cords Vascular communication between fetuses 9. artery-to-artery.OUTCOMES OF MULTIFETAL PREGNANCY 8. most vascular communications are hemodynamically balanced and of little fetal consequence ie.
monozygotic multiple gestation normally formed donor twin with features of heart failure Recipient twin recipient twin without a normal heart (acardius) and missing other structures. acephalus .OUTCOMES OF MULTIFETAL PREGNANCY a) Acardiac twin – TRAP (Twin reversedarterial-perfusion) sequence complication of monochorionic. ie.
Defects from vascular interchange: ACARDIA .B.
OUTCOMES OF MULTIFETAL PREGNANCY b) Twin-to-twin transfusion syndrome Blood from donor twin to recipient twin donor develops anemia and IUGR recipient has polycythemia with circulatory overload hydrops donor twin is pale. recipient is plethoric .
oligohydramnios or stuck twin (in donor sac) Hemoglobin difference >5 g/dL POSTNATAL Diagnosed postnatally: weight discordance of 15 or 20% Hgb difference > 5 g/dL with the smaller twin being anemic .Twin-to-twin transfusion syndrome ANTENATAL Same sex fetuses Monochorionicity with placental vascular connections Intertwin weight difference >20% Hydramnios in the large twin.
Discordant twin unequal size of twin fetuses sign of pathological growth restriction in one fetus defined using larger twin as the index direct proportional increase in perinatal mortality as weight difference within twin increases .OUTCOMES OF MULTIFETAL PREGNANCY 10.
and time interval between demise and delivery of surviving twin FETUS PAPYRACEOUS . the chorionicity.OUTCOMES OF MULTIFETAL PREGNANCY 13. Death of one (or two) twin(s) maternal risk and prognosis for the surviving twin depend on the gestational age the time of the demise.
Complete hydatidiform mole and coexisting fetus Two separate conceptuses: a normal placenta in one twin and a complete molar gestation in the other Management is uncertain .OUTCOMES OF MULTIFETAL PREGNANCY 14.
vitamins and essential fatty acids are increased.MANAGEMENT OF MULTIFETAL PREGNANCY 1. minerals. Antenatal Dietary requirements for calories. proteins. Hypertension Prevention of preterm labor and delivery: bed rest tocolytic therapy prophylactic cervical cerclage. .
abnormal presentations prolapse of the umbilical cord premature separation of the placenta immediate postpartum hemorrhage . cephalic-breech. Labor and delivery Fetal presentation and position cephalic-cephalic. uterine dysfunction. and cephalictransverse Conduct of labor and delivery: preterm labor.MANAGEMENT OF MULTIFETAL PREGNANCY 2.
Labor and delivery Route of delivery by fetal presentation: Cephalic-cephalic – vaginal Cephalic-noncephalic – controversial Breech or transverse first of twin – abdominal Anesthesia: epidural provides pain relief skeletal muscle relaxation required for internal podalic version rapidly extended cephalad if CS required .MANAGEMENT OF MULTIFETAL PREGNANCY 2.
Postterm Pregnancy .
Postterm Pregnancy Postterm pregnancy – >42 completed weeks (294 days) from LMP Postmaturity – infant clinical features indicating a pathologically prolonged pregnancy .
thin body suggesting wasting advanced maturity: open-eyed.Pathophysiology Postmaturity syndrome – postmature infant with characteristic appearance: wrinkled. patchy peeling skin. unusually alert. old and worried-looking attributed to placental senescence . long.
Pathophysiology Oligohydramnios due to decreased amniotic fluid volume consequence of cord compression associated with oligohydramnios Fetal distress Fetal release of meconium in reduced amniotic fluid thick. viscous meconium thick. viscous meconium Fetal growth restriction in 1/3 of cases .
amniotic fluid determinations Prostaglandin gels Use of oxytocin Cervical ripening Induction of labor .Management Antenatal surveillance Nonstress tests.
Inappropriate fetal growth Baby too small Baby too big .
3 PHASES OF FETAL GROWTH 1. >32 weeks hypertrophy with fetal fat and glycogen deposition 30-35 g/day . 1st 16 weeks gestation hyperplasia 5 gram/day 2. 16-32 weeks hyperplasia and hypertrophy 15-20 g/day 3.
2. synthesized in adipose tissue Maternal glucose: excessive glycemia causes macrosomia. IGF-II) – cell division and differentiation Leptin – correlates with birthweight. decreased glycemia causes growth restriction 3. Genetics Hormones Insulin – somatic growth and adiposity Insulin-like growth factors (IGF-I. Nutrition .Factors that influence fetal growth 1.
FETAL GROWTH RESTRICTION Small for gestational age Birthweight <10th percentile for gestational age At risk for fetal death 0.2% for normal 38 weekers vs 2% for SGAs Uteroplacental isufficiency .
Complications of SGA babies Fetal demise Asphyxia Meconium aspiration Neonatal hypoglycemia Hypothermia Abnormal neurological development .
Preferential shunting of oxygen and nutrients to brain Early insult from viral infection. low apgar score . chemical exposure.Symmetrical FGR Head to abdomen circumference ratio (HC/AC) Ratio >95% percentile Asymmetric fetus had bigger brain. operative intervention. fetal distress. protected from full effects of growth retarding stimulus. aneuploidy affecting cellular number an size Severe preeclampsia.
Asymmetrical FGR Late insult: uteroplacental insufficiency affecting cell size Hypertension .
Risk factors 1. smoking. Social deprivation . alcohol. Poor maternal weight gain and nutrition 3. Constitutionally small mothers Mother <100 lbs with two-fold increase in risk for SGA Weight gain during pregnancy Lifestyle and use of illicit substances. nutrition 2.
f. e. decreased rate of cell division Hepatitis A and B Listeriosis Tuberculosis Syphilis –megaplacenta due to edema and perivascular inflammation Toxoplasmosis Congenital malaria . c. b. d. h.Risk factors 4. g. Fetal infections a. Cytomegalovirus – direct cytolysis and loss of functional cells Rubella – vascular insufficiency endothelial cell damage.
16) – reduced number of small arteries in tertiary villi uteroplacental insufficiency and abnormal cell growth and differentiation 6. 18. 13. Congenital malformations Primary disorders of bone and cartilage . Chromosomal abnormalities Autosomal trisomies (21.Risk factors 5. 7.
Risk factors 8. Chemical teratogens Anticonvulsants: phenytoin and trimethadione Narcotics Smoking Alcohol Cocaine .
13. Vascular disease Chronic renal disease Chronic hypoxia Maternal anemia Placental and cord abnormalities Chronic placental separation Infarction Chorioangioma . 11. 10. 12.Risk factors 9.
Multiple gestation APAS – vascular thrombosis. 15. maternal platelet aggregation and placental thrombosis Anticardiolipin antibody Lupus anticoagulant 16.Risk factors 14. Extrauterine pregnancy .
SCREENING AND DIAGNOSIS 1. 3. fundic height in cm = gestation in weeks +1 cm 4. Identify risk factors history of growth retarded fetus . Establish gestational age Maternal weight gain Uterine fundal growth Normal: 18-30 weeks. 2.
Doppler velocimetry .SCREENING AND DIAGNOSIS 5. Serial sonographic measurements of head. abdominal. femoral Abdominal circumference is most reliable Umbilical artery – absent or reversed flow increased impedance IUGR Adjunct to NST and BPP 6.
Management of Growth Restricted Fetus Look for congenital malformations Determine if fetus is in poor condition Cordocentesis for karyotyping Lethal aneupliody Weigh risk of fetal death vs preterm delivery .
Expectant management Fetal well being studies . Prompt delivery: >34 weeks Reassuring FHR pattern: vaginal delivery Fetal distress: CS 2.FGR near TERM 1.
With fetal growth allow pregnancy to continue Fetal compromise Deliver .FGR remote from TERM 1. 3. <34 weeks + normohydramnios + normal fetal surveillance Observation Fetal surveillance every 2-3 weeks Amniocentesis for fetal lung maturity 2.
FGR remote from TERM Bed rest. LLD position Nutritional supplementation Hydration Oxygen therapy Medications Antihypertensive drugs Aspirin Heparin Dipyridamole Nitrol patch .
Labor and Delivery of Growthrestricted Fetus Continuous fetal heart rate pattern surveillance Uteroplacental insufficiency Oligohydramnios cord compression Meconium aspiration Hypothermia Polycythemia and hyperviscosity Hypoglycemia .
DISEASES and INJURIES of the FETUS and the NEWBORN
HYALINE MEMBRANE DISEASE
Etiology: inadequate surfactant production by type II pneumonocytes
Signs and symptoms
tachypnea and chest wall retraction expiration is accompanied by a whimper and grunt (combination of “grunting and flaring
HYALINE MEMBRANE DISEASE
chest x-ray: diffuse reticulogranular infiltrate with an air-filled tracheobronchial tree (air bronchogram)
HYALINE MEMBRANE DISEASE Complications bronchopulmonary dysplasia pulmonary hypertension retinopathy of prematurity .
HYALINE MEMBRANE DISEASE Continuous positive airway pressure (CPAP) prevents collapse of unstable alveoli Surfactant prophylaxis of preterm infants at risk for RDS Rescue for those with established disease .
RETINOPATHY OF PREMATURITY Retinal vessels damaged by excessive oxygen Oxygen induces severe vasoconstriction. endothelial damage and vessel obliteration .
MECONIUM ASPIRATION Peripartum inhalation of meconium-stained amniotic fluid inflammation of pulmonary tissues and hypoxia May progress to persistent pulmonary hypertension. morbidity and death Pregnancies at risk for meconium aspiration Oligohydramnios Cord compression Uteroplacental insufficiency .
MECONIUM ASPIRATION Chest X ray .
particulate meconium is placed on radiant warmer .MECONIUM ASPIRATION Prevention Suction infant’s mouth and nares before shoulders are delivered Suction under direct visualization as soon as infant who has passed thick.
hypoxia in preterm infants Periventricular-intraventricular hemorrhage Unknown cause in 25% of cases .INTRAVENTRICULAR HEMORRHAGE Etiology Subdural hematoma – trauma Subarachnoid and intracerebellar hemorrhage – trauma in term infants.
INTRAVENTRICULAR HEMORRHAGE .
INTRAVENTRICULAR HEMORRHAGE Patholophysiology: damage to the germinal matrix capillary network extravasation of blood into the surrounding tissues capillary network is fragile in preterm infants Periventricular leukomalacia Neurodevelopmental handicaps Long term sequelae Treatment: corticosteroids before delivery appears to prevent intraventricular hemorrhage in preterm infants .
CEREBRAL PALSY Nonprogressive motor disorder of early infancy involving > 1 limbs resulting from muscular spasticity or paralysis Types Spastic quadriplegia Diplegia Hemiplegia Choreoathetoid type Mixed varieties .
Genetic abnormalities such as maternal mental retardation. 3.CEREBRAL PALSY Risk factors 1. microcephaly. congenital malformations Birthweight l< 2000 grams 2. Gestational age <32 weeks Infection Correlation with intrapartum asphyxia controversial . 4.
subnormal level of consciousness and frequently seizures Believed to be a consequence of an hypoxicischemic insult . depressed tone and reflexes.NEONATAL ENCEPHALOPATHY Syndrome of disturbed neurological function in the earliest days of life in term infant Consists of difficulty in initiating and maintaining respiration.
ANEMIA Cord hemoglobin < 14 g/dl (>35 weeks. mean cord hemoglobin concentration = 17 g/dL) Hemoglobin due to delayed cord clamping appreciable volume of blood being expressed from the placenta through the cord of the infant Hemoglobin if placenta is cut or torn. or the infant is held well above the level of the placenta before cord clamping . a fetal vessel is perforated or lacerated.
such as neonatal jaundice or anemia but not erythroblastosis fetalis Treatment: Phototherapy .ABO INCOMPATIBILITY Incompatibility for the major blood group antigens A and B is the most common cause of hemolytic disease of the newborn Invariably causes mild disease.
IMMUNE HYDROPS Subcutaneous edema Effusion into the serous cavities presence of abnormal fluid in > 2 sites such as thorax. Edematous placenta. enlarged and boggy . abdomen or skin.
Portal and umbilical venous hypertension from hepatic parenchymal disruption by extramedullary hematopoiesis Decreased colloid oncotic pressure from hypoproteinemia caused by liver dysfunction .IMMUNE HYDROPS Pathophysiology: obscure Theories Heart failure and capillary leakage from profound anemia.
or evacuation of a molar or ectopic pregnancy Prevention: . subsequent management is individualized anti-D immunoglobulin to Rh(-) women at 28 weeks. abortion.IMMUNE HYDROPS Treatment: identify woman at risk at first prenatal appointment After identification of isoimmunization and the fetus at risk for optimal outcome. and after delivery if the infant is D-positive Immunoglobulin given to Rh(-) women after miscarriage.
NONIMMUNE HYDROPS Etiology cardiac abnormalities fetal heart failure chromosomal abnormalities twin-to-twin transfusion syndrome severe anemia inborn errors of metabolism anomalous lymph system Treatment depends on the cause .
IX and X) Etiology Prevention: Vit K 1 mg IM at delivery dietary vitamin K deficiency – main cause Hemophilia congenital syphilis Sepsis thrombocytopenia purpura erythroblastosis intracranial hemorrhage .HEMORRHAGIC DISEASE of the NEWBORN Spontaneous internal or external bleeding accompanied by hypoprothrombinemia & very low levels of other vitamin K-dependent coagulation factors (V. VII.
ileus and bloody stools Seen in low birthweight infants .NECROTIZING ENTEROCOLITIS Clinical findings: abdominal distention.
NECROTIZING ENTEROCOLITIS Radiologic evidence: pneumatosis intestinalis caused by intestinal wall gas from invasion by gasforming bacteria and bowel perforation .
intrapartum asphyxia twin-to-twin transfusion chorioamnionitis Unexplained (25-35%) APAS DM Hypertension Trauma Abnormal labor Sepsis Acidosis.FETAL DEATH Fetal causes (25-40%) chromosomal anomalies nonchromosomal birth defects nonimmune hydrops infections Maternal (5-10%) Uterine rupture Postterm pregnancy Drugs Placental causes (2535%) Abruption. previa fetal-maternal hemorrhage cord accident placental insufficiency. hypoxia .
INJURIES of the FETUS and NEWBORN .
subarachnoid. cortical. bridging veins from the cerebral cortex to the sagittal sinus may tear Causes Birth trauma during difficult labor and delivery Prenatal factors: genetic and environmental .Intracranial hemorrhage Sites: subdural. cerebellar. and periventricular Most common type: IC bleed in the germinal matrix Severe molding & overlapping of parietal bones. intraventricular. white matter.
often growing larger and disappearing only after weeks or even months .CEPHALHEMATOMA Injury to periosteum of the skull during labor and delivery Periosteal limitations. definite palpable edges May not appear for hours after delivery.
then grows smaller Usually disappears within a few hours if small. and within a few days if very large .CAPUT SUCCEDANEUM Focal swelling of the scalp from edema that overlies the periosteum Maximal at birth.
CAPUT SUCCEDANEUM vs CEPHALHEMATOMA CAPUT SUCCEDANEUM CEPHALHEMATOMA .
NERVE INJURIES Spinal injury – overstretching the spinal cord and associated hemorrhage following excessive traction during a breech delivery .
NERVE INJURIES Brachial plexus injury – Duchenne paralysis results from stretching or tearing of the upper roots of the brachial plexus .
NERVE INJURIES Facial paralysis – seen with delivery of an infant in which head has been seized obliquely with forceps .
FRACTURES Fractures Clavicular Humeral Femoral Skull fractures .
CONGENITAL MALFORMATIONS AND INHERITED DISEASES .
Women at risk for fetal aneuploidy 1. 4. Previous pregnancy with autosomal trisomy 1% occurrence. 2. Previous pregnancy with triple XXX (47XXX) or Klinefelter syndrome 47 XXY Extra X may be maternal or paternal 47 XYY and 45 X not at high risk for recurrence . Women with singleton pregnancy at least age 35 at delivery Women with dizygotic twin pregnancy at least age 31 at delivery Risk for fetal Down syndrome – 1:190 3. until age-related risk >1.
History of triploidy Recurrence risk is 1 – 1.5% if fetus survives 1st trimester . Woman or partner who is a translocation carrier. 5 – 30% risk 6. Woman or partner who is a chromosomal inversion carrier. 5 – 10% risk 7.Women at risk for fetal aneuploidy 5.
Women at risk for fetal aneuploidy 8. 47.XYY have 30% risk of having trisomic offspring Detect it through maternal and paternal karyotyping 10.XXX and 47. Repetitive spontaneous 1st trimester losses Karyotype on the parents most useful 9. Fetus with major structural defect identified by ultrasound . Parental aneuploidy Trisomy 21.
drug use Mother > 2 siblings > 1 sibling > father Recurrence risk for CHD: Prenatal diagnosis: fetal 2D echocardiogram at 20 – 22 weeks gestation . smoking. 7:1000 births Etiology Genetic Environmental – DM. poor OB history.Congenital Heart Disease Most common birth defect. viral infections.
Congenital Heart Disease PDA ASD .
Congenital Heart Disease TETRALOGY OF FALLOT TRICUSPID ATRESIA .
Neural Tube Defects Family history of neural tube defects most important risk factor Risk to 10 relative 2-3%. # of relatives affected Period of risky exposure: 1st 28 days gestation Hyperglycemia Hyperthermia Drugs: carbamazepine. related to degree of relations. isotretinoin Exposure to environmental agents . valproic acid. aminopterin.
Roberts-SC phocomelia Known high-risk racial.Neural Tube Defects NTDs as part of a genetic syndrome with known recurrence risk Inherited syndromes: Meckel-Gruber. ethnic groups or living in high-risk geographic areas UK – highest incidence Sikhs in India > Sikhs in Canada .
>2.0-2. banana sign Risk of NTD reduced by 95% if none found by UTZ Amniocentesis for AF aFP NTD suspect with elevated aFP but (-) UTZ Elevated serum and AF aFP. do karyotyping .5 MOM Major cranial. spinal defects can be detected Targeted ultrasound Lemon sign.Screening for NTDs Maternal serum a-fetoprotein At 15-22 weeks gestation.
Ultrasound-guided AMNIOCENTESIS .
Neural Tube Defects ANENCEPHALY INIENCEPHALY .
Neural Tube Defects
Majority of Down syndrome pregnancies are de novo and in women age <35. Maternal age – most important risk factor Multiple marker screening
Low a-fetoprotein Elevated b-human chorionic gonadotrophin Decreased unconjugated estriol
Long face.FRAGILE X SYNDROME Most common cause of familial mental retardation Affected female carriers are normal. elongated ears. . testes larger than normal.
liver disease.CYSTIC FIBROSIS Autosomal Recessive 1:25 Euro Caucasians Abnormal sweat chloride level. chr pulmonary disease. obstructive azoospermia Pregnancy termination . pancreatic insufficiency.
CONGENITAL DIAPHRAGMATIC HERNIA 1:3700 Fetal surgical correction to restore normal intrathoracic anatomy and allow pulmo dev’t prevent pulmo hypoplasia .
conjoined twins. hydrocephalus Intrauterine fetal therapy Pulmonary immaturity – transplacental glucocorticoids Intrauterine growth restriction – protein-calores .g.Management of fetuses with congenital anomalies Team approach Route of delivery CS if malformation will cause dystocia e.
chest wall and extremity deformities . hydronephrosis Hydrops IUGR Intestinal ischemia Volvulus Meconium ileus GIT atresias Meconium ileus Small meningocoele.Management of fetuses with congenital anomalies Malformations needing early correction ex utero Malformations best corrected in term infant Obstructive hydrocephalus. spina bifida Smal sacrococcygeal teratoma Craniofacial.
OBSTETRIC COMPLICATIONS Maternal and fetal conditions that make the pregnancy at risk for morbidity and mortality: Premature rupture of membranes Congenital malformations and inherited diseases Diseases and injuries of the fetus and the newborn infant Multifetal pregnancy Preterm labor Postterm pregnancy Inappropriate fetal growth Definition Risk factors Pathophysiology Management .
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