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OBSTETRIC OBSTETRIC COMPLICATIONCOMPLICATION
SS
Ma. Bernadette O. Cruz, MD, MSc, FPOGSMa. Bernadette O. Cruz, MD, MSc, FPOGS
OBSTETRIC OBSTETRIC COMPLICATIONSCOMPLICATIONS
Selected maternal and fetal conditions that make Selected maternal and fetal conditions that make the pregnancy at risk for maternal and fetal the pregnancy at risk for maternal and fetal morbidity and mortality.morbidity and mortality. Multifetal pregnancyMultifetal pregnancy Preterm laborPreterm labor Postterm pregnancyPostterm pregnancy Inappropriate fetal growthInappropriate fetal growth Premature rupture of membranesPremature rupture of membranes Congenital malformations and inherited diseasesCongenital malformations and inherited diseases Diseases and injuries of the fetus and the newborn Diseases and injuries of the fetus and the newborn
infantinfant
VARIATIONS IN THE VARIATIONS IN THE DURATION OF PREGNANCYDURATION OF PREGNANCY
Average duration of normal Average duration of normal pregnancypregnancy 260 days from conception260 days from conception 280280++14 days from LMP 14 days from LMP
Incidence of preterm birth - 5% of Incidence of preterm birth - 5% of pregnancies (<36 weeks) pregnancies (<36 weeks)
10% of cases, the pregnancy is 10% of cases, the pregnancy is prolonged. prolonged. birth >41 weeks birth >41 weeks
Preterm Labor and DeliveryPreterm Labor and Delivery
Preterm DeliveryPreterm Delivery
Preterm – infants delivered before Preterm – infants delivered before completion of 37 weeks (259th day)completion of 37 weeks (259th day)
Low birthweight – <2500 gramsLow birthweight – <2500 grams
Very low birthweight – Very low birthweight – <<1500 grams1500 grams
Extremely-low birthweight – Extremely-low birthweight – <<1000 1000 grams grams
Etiology of preterm laborEtiology of preterm labor
1.1. Medical and Medical and obstetric obstetric complicationscomplications
a.a. PreeclampsiaPreeclampsiab.b. fetal distressfetal distressc.c. fetal growth fetal growth
restrictionrestrictiond.d. abruptio placentaeabruptio placentaee.e. fetal deathfetal deathf.f. spontaneous spontaneous
preterm laborpreterm labor
2.2. Lifestyle factorsLifestyle factorsa.a. low prepregnancy weightlow prepregnancy weight
b.b. smokingsmoking
c.c. alcohol abusealcohol abuse
d.d. Young gravida Young gravida
e.e. PovertyPoverty
f.f. short statureshort stature
g.g. occupational factorsoccupational factors
h.h. psychological stresspsychological stress
Etiology of preterm laborEtiology of preterm labor
3.3. Genetic factorsGenetic factors
4.4. Amnionic fluid and chorioamnionic Amnionic fluid and chorioamnionic infectioninfection
initiated by secretory products initiated by secretory products (interleukin-1, tumor necrosis factor, (interleukin-1, tumor necrosis factor, interleukin-6) resulting from monocyte interleukin-6) resulting from monocyte activation in response to infectionactivation in response to infection
Phospholipase A Phospholipase A cleaves arachidonic cleaves arachidonic acid acid prostaglandin synthesis prostaglandin synthesis
Etiology of preterm laborEtiology of preterm labor
5.5. Epidemiologic studies: Low SES, Epidemiologic studies: Low SES, nonwhite race, maternal age <18 nonwhite race, maternal age <18 years or >40 years, low years or >40 years, low prepregnancy weight.prepregnancy weight.
6.6. Multiple gestation – although Multiple gestation – although incidence is only 1.1%, MP accounts incidence is only 1.1%, MP accounts for 10% of all preterm birthsfor 10% of all preterm births
Etiology of preterm laborEtiology of preterm labor
7.7. History of preterm birth History of preterm birth Recurrence risk: of 17-37%Recurrence risk: of 17-37%
Risk increases with number of preterm births Risk increases with number of preterm births and decreases with number of term and decreases with number of term deliveries.deliveries.
7.7. Risk of preterm birth increases with Risk of preterm birth increases with women who had spontaneous second-women who had spontaneous second-trimester abortion(s).trimester abortion(s).
8.8. No PNC regardless of SESNo PNC regardless of SES
Etiology of preterm laborEtiology of preterm labor
10.10. Coitus and orgasm (?); sexual Coitus and orgasm (?); sexual abstinence in the prevention of abstinence in the prevention of preterm labor (?).preterm labor (?).
11.11. PROMPROM
12.12. Uterine malformations – unicornuate Uterine malformations – unicornuate and bicornuate uteriand bicornuate uteri
13.13. Uterine myoma – submucosal or Uterine myoma – submucosal or subplacentalsubplacental
Etiology of preterm laborEtiology of preterm labor
14.14. Cervical incompetence Cervical incompetence 0.1-2% of all pregnancies 0.1-2% of all pregnancies due to trauma from prior obstetric or due to trauma from prior obstetric or
gynecologic procedure, gynecologic procedure, diethylstilbestrolexposure in uterodiethylstilbestrolexposure in utero
14.14. Infectious causesInfectious causes STDsSTDs ChorioamnionitisChorioamnionitis Group B streptococci, N. gonorrhoeae, C. Group B streptococci, N. gonorrhoeae, C.
trachomatis, U. urealyticum, T. pallidum, T. trachomatis, U. urealyticum, T. pallidum, T. vaginalis or G vaginalis.vaginalis or G vaginalis.
Signs and symptomsSigns and symptoms
Painful or painless uterine contractions, Painful or painless uterine contractions, pelvic pressurepelvic pressure
Watery or bloody vaginal dischargeWatery or bloody vaginal discharge Menstrual-like cramps and low back painMenstrual-like cramps and low back pain Asymptomatic cervical dilatation after Asymptomatic cervical dilatation after
midpregnancy midpregnancy mean cervical length (UTZ) at 24 weeks = 35 mmmean cervical length (UTZ) at 24 weeks = 35 mm
women with progressively shorter cervices women with progressively shorter cervices experienced increased rates of preterm birthexperienced increased rates of preterm birth
Diagnostics: 1. Fetal fibronectinDiagnostics: 1. Fetal fibronectin A glycoprotein produced by fetal amnion, A glycoprotein produced by fetal amnion,
hepatocytes, malignant cells, fibroblasts, hepatocytes, malignant cells, fibroblasts, endothelial cellsendothelial cells
Plays a role in intercellular adhesion: Plays a role in intercellular adhesion: implantation, adhesion of placenta to implantation, adhesion of placenta to deciduadecidua
Detection of fetal fibronectin in Detection of fetal fibronectin in cervicovaginal secretions prior to cervicovaginal secretions prior to membrane rupture may be a marker for membrane rupture may be a marker for impending preterm laborimpending preterm labor
DiagnosticsDiagnostics
2.2. Ambulatory uterine contraction Ambulatory uterine contraction testing – use of home monitoring of testing – use of home monitoring of uterine contractions for prevention uterine contractions for prevention of preterm labor controversialof preterm labor controversial
3.3. maternal salivary estriol maternal salivary estriol associated with preterm deliveryassociated with preterm delivery
CRITERIA FOR DIAGNOSISCRITERIA FOR DIAGNOSIS ((American Academy of Pediatrics and the American American Academy of Pediatrics and the American College of Obstetricians and Gynecologists, 1997)College of Obstetricians and Gynecologists, 1997)
1.1. Contractions occurring at a Contractions occurring at a frequency of four in 20 minutes or frequency of four in 20 minutes or eight in 60 minutes + progressive eight in 60 minutes + progressive change in the cervixchange in the cervix
2.2. Cervical dilatation > 1 cmCervical dilatation > 1 cm
3.3. Cervical effacement of Cervical effacement of >> 80% 80%
ManagementManagement
1.1. Gestational age?Gestational age?
2.2. Condition of membranes? Condition of membranes?
Successful treatment achieved Successful treatment achieved when initiated early, before when initiated early, before advanced cervical dilatation and advanced cervical dilatation and rupture of membranesrupture of membranes
1.1. Premature labor with intact Premature labor with intact membranesmembranes
A.A. Glucocorticoid therapyGlucocorticoid therapy Corticosteroids accelerate lung maturation Corticosteroids accelerate lung maturation
lower incidence of RDS, mortality from lower incidence of RDS, mortality from hyaline membrane diseasehyaline membrane disease
Induction of proteins that regulate Induction of proteins that regulate biochemical systems within type II cells in biochemical systems within type II cells in the fetal lung to produce surfactantthe fetal lung to produce surfactant
A.A. Cervical cerclage – in recurrent Cervical cerclage – in recurrent midtrimester lossesmidtrimester losses
Premature labor with intact Premature labor with intact membranesmembranes
C.C. Treat bacterial vaginosis linked to increased Treat bacterial vaginosis linked to increased preterm birth at preterm birth at <<32 weeks or less32 weeks or less
treatment of asymptomatic BV did not improve treatment of asymptomatic BV did not improve pregnancy outcomespregnancy outcomes
Other vaginal infections: trichomoniasis, chlamydial Other vaginal infections: trichomoniasis, chlamydial
C.C. Bed rest Bed rest most often used treatment regimenmost often used treatment regimen
no conclusive evidence that bed rest is effective no conclusive evidence that bed rest is effective
C.C. Hydration and sedation Hydration and sedation
Premature labor with intact Premature labor with intact membranesmembranes
F.F. TocolysisTocolysis
1.1. Beta-adrenergic receptor agonistsBeta-adrenergic receptor agonists
2.2. Magnesium sulfateMagnesium sulfate
3.3. Prostaglandin inhibitorsProstaglandin inhibitors
4.4. Calcium channel blockersCalcium channel blockers
Tocolytic AgentsTocolytic Agents
DRUGSDRUGS MechanismMechanism Side Side EffectsEffects
ExampleExample
ββ -adrenergic -adrenergic receptor receptor agonistagonist
Combines w/ Combines w/ receptor to receptor to activate adenyl activate adenyl cyclase w/c cyclase w/c converts ATP to converts ATP to cAMP; decreases cAMP; decreases intracellular CAintracellular CA+ + prevents prevents contractioncontraction
Pulmo edema, Pulmo edema, inc. capillary inc. capillary permeability, permeability, arrhythmia, arrhythmia, myocardial myocardial ischemiaischemia
Ritodrine, Ritodrine,
terbutalineterbutaline
Magnesium Magnesium sulfate sulfate
blocks calcium influx blocks calcium influx at membrane, at membrane, activates adenylate activates adenylate cyclase, increases cyclase, increases cAMP which reduces cAMP which reduces intracellular calcium intracellular calcium
Hyporeflexia at Hyporeflexia at 6-12 6-12 mEq/L, Loss of mEq/L, Loss of DTRs at 10 DTRs at 10 mEqs, mEqs, Respiratory Respiratory paralysis at 15 paralysis at 15 mEqsmEqs
Cardiac arrest at Cardiac arrest at 25 mEqs25 mEqs
Tocolytic AgentsTocolytic Agents
DRUGSDRUGS MechanismMechanism Side Side EffectsEffects
ExampleExample
Prostaglandin Prostaglandin inhibitorinhibitor
inhibits synthesis inhibits synthesis of PGs, blocks of PGs, blocks action of PGs on action of PGs on target organs; target organs; PGs are involved PGs are involved in myometrial in myometrial contractions of contractions of normal labornormal labor
closure of closure of ductus ductus arteriosus, arteriosus, necrotizing necrotizing enterocolitis, enterocolitis, intracranial intracranial hemorrhage hemorrhage
Indomethacin, Indomethacin, sulindacsulindac
Calcium Calcium channel channel blockersblockers
inhibit entry of inhibit entry of CA+ thru cell CA+ thru cell membrane membrane channels channels reduction in CA+ reduction in CA+ concentration concentration inhibits inhibits contractioncontraction
maternal maternal hypotension hypotension and decreased and decreased uteroplacental uteroplacental perfusion, perfusion, tachycardiatachycardia
NifedipineNifedipine
Tocolytic AgentsTocolytic Agents
DRUGSDRUGS MechanismMechanism Side Side EffectsEffects
ExampleExample
AtosibanAtosiban oxytocin analog; oxytocin analog; competitive competitive oxytocin-oxytocin-vasopressin vasopressin antagonistantagonist
Nitric oxideNitric oxide potent potent endogenous endogenous smooth-smooth-muscle muscle relaxantrelaxant
ManagementManagement
2.2. Preterm labor + preterm premature Preterm labor + preterm premature rupture of membranes (PPROM)rupture of membranes (PPROM)
Expectant management or Expectant management or nonintervention – spontaneous labor is nonintervention – spontaneous labor is simply awaitedsimply awaited
Corticosteroids Corticosteroids ++ tocolytic agents to tocolytic agents to allow corticosteroids to work (induce allow corticosteroids to work (induce fetal lung maturation)fetal lung maturation)
Premature rupture of Premature rupture of membranes (PROM)membranes (PROM)
Premature rupture of Premature rupture of membranesmembranes
Rupture of membranes before onset of laborRupture of membranes before onset of labor Incidence: 8-10%Incidence: 8-10%
25% of cases the fetus is preterm.25% of cases the fetus is preterm.
Preterm premature rupture of membranes – Preterm premature rupture of membranes – rpture of membranes before onset of labor rpture of membranes before onset of labor at gestational age <37 weeks.at gestational age <37 weeks.
Prolonged rupture of membranes – PROM Prolonged rupture of membranes – PROM >24 hours before delivery.>24 hours before delivery.
Latency period – time between PROM and Latency period – time between PROM and onset of labor.onset of labor.
Amniotic fluid is necessary for normal Amniotic fluid is necessary for normal fetal lung development. fetal lung development.
It also protects the fetus from trauma It also protects the fetus from trauma and umbilical cord from compression. and umbilical cord from compression.
RUPTURE OF MEMBRANES
OLIGOHYDRAMNIOSOLIGOHYDRAMNIOS
Premature rupture of Premature rupture of membranesmembranes
May lead to onset of preterm laborMay lead to onset of preterm labor
In most cases, the baby is born In most cases, the baby is born within 7 days of the prelabor rupture. within 7 days of the prelabor rupture.
Prolonged PROM increases risk for Prolonged PROM increases risk for chorioamnionitis. chorioamnionitis.
Risk factors for PROMRisk factors for PROM1.1. Local infection – weakening of Local infection – weakening of
membranesmembranes N. gonorrhoeae, C. trachomatis, Group B N. gonorrhoeae, C. trachomatis, Group B
strep, T. vaginalis, G. vaginalisstrep, T. vaginalis, G. vaginalis
1.1. PolyhydramniosPolyhydramnios2.2. Incompetent cervixIncompetent cervix3.3. Cervical cerclageCervical cerclage4.4. Previous cervical laceration or Previous cervical laceration or
operationoperation5.5. SmokingSmoking
Clinical presentationClinical presentation
Gush of fluid from the vagina Gush of fluid from the vagina followed by persistent leakage of followed by persistent leakage of fluid (90%)fluid (90%)
Differentiate from urine, excessive vaginal Differentiate from urine, excessive vaginal discharge or mucus, bloody show discharge or mucus, bloody show associated with laborassociated with labor
ChorioamnionitisChorioamnionitis
Preterm laborPreterm labor
DiagnosticsDiagnostics
1.1. Tests to document rupture of Tests to document rupture of membranesmembranes
Nitrazine test for pH of vaginaNitrazine test for pH of vagina Normal vaginal pH: 4.5 – 6Normal vaginal pH: 4.5 – 6 AF pH: 7.1 – 7.3AF pH: 7.1 – 7.3 Nitrazine paper: yellow Nitrazine paper: yellow blue pH >6.0 blue pH >6.0
Microscopic slide test for ferning of Microscopic slide test for ferning of vaginal fluidvaginal fluid (+) ferning with AF(+) ferning with AF
DiagnosticsDiagnostics
2.2. Ultrasound examinationUltrasound examination Establish AOGEstablish AOG
Fetal presentationFetal presentation
Low AF indexLow AF index
2.2. Cervical culturesCervical cultures
DiagnosticsDiagnostics4.4. Tests to rule out chorioamnionitis Tests to rule out chorioamnionitis
a.a. CBC with differentialCBC with differential
b.b. Serum C-reactive protein >0.8 mg/dlSerum C-reactive protein >0.8 mg/dl
c.c. Amniocentesis and AF cultureAmniocentesis and AF culture
d.d. Biophysical profileBiophysical profile
a.a. Fetal breathing movementsFetal breathing movements
b.b. Gross body movementGross body movement
c.c. Fetal toneFetal tone
d.d. Reactive FHRReactive FHR
e.e. Qualitattive AFVQualitattive AFV
DiagnosticsDiagnostics5.5. Tests for fetal lung maturityTests for fetal lung maturity
a.a. Fetal lung maturity – impt factor in PROMFetal lung maturity – impt factor in PROM
b.b. Lecithin-sphingomyelin (L/S) ratio >2Lecithin-sphingomyelin (L/S) ratio >2
c.c. (+) Phosphatidylglycerol(+) Phosphatidylglycerol
d.d. Foam stability test – shake testFoam stability test – shake test
a.a. AF with sufficient surfactant forms stable stable AF with sufficient surfactant forms stable stable foam at air-surface interface for 15 minfoam at air-surface interface for 15 min
a.a. High false-negatives: LS ratio 4-6High false-negatives: LS ratio 4-6
Complications from PROMComplications from PROMThreats to the fetusThreats to the fetus
1.1. PrematurityPrematurity Responsible for 30% of all preterm births Responsible for 30% of all preterm births
(>low SES, STD)(>low SES, STD) PROM at term: 90% of patients will go into PROM at term: 90% of patients will go into
labor <24 hourslabor <24 hours PPROM 28-34 weeks AOG: 50% in labor PPROM 28-34 weeks AOG: 50% in labor
within 24 hours; 80-90% within 1 weekwithin 24 hours; 80-90% within 1 week PPROM <26 weeks: 50% in labor within 1 PPROM <26 weeks: 50% in labor within 1
weekweek
Complications from PROMComplications from PROMThreats to the fetusThreats to the fetus
2.2. InfectionInfection Serous infection: 5% of preterm PROM Serous infection: 5% of preterm PROM
15-20% with chorioamnionitis15-20% with chorioamnionitis Fetal pneumonia, sepsis, UTI, Fetal pneumonia, sepsis, UTI,
conjunctivitisconjunctivitis
2.2. Fetal distressFetal distress Incidence: 8.5% (6-fold increase in Incidence: 8.5% (6-fold increase in
risk)risk) Umbilical cord compression or Umbilical cord compression or
prolapseprolapse
Complications from PROMComplications from PROMThreats to the fetusThreats to the fetus
Fetal deformationsFetal deformations Early preterm PROM: impaired feltal Early preterm PROM: impaired feltal
lung development lung development pulmonary pulmonary hypoplasiahypoplasia
IUGRIUGR
Compression malformations of face Compression malformations of face and limbs (3.5%) and limbs (3.5%)
esp <26 weeks AOG esp <26 weeks AOG
Complications from PROMComplications from PROMThreats to the Mother Threats to the Mother
Sepsis secondary to Sepsis secondary to chorioamnionitis Overall: 0.5-1%. chorioamnionitis Overall: 0.5-1%.
Prolonged PROM chorioamnionitis: Prolonged PROM chorioamnionitis: 3-15%. 3-15%.
Preterm PROM: 15-25%Preterm PROM: 15-25%
Management of PROMManagement of PROM
1.1. PROM + advanced labor, PROM + advanced labor, chorioamnionitis, fetal distress chorioamnionitis, fetal distress regardless of gestationregardless of gestation
Vaginal deliveryVaginal delivery CS for obstetric reasonsCS for obstetric reasons Antibiotic treatmentAntibiotic treatment
AmpicillinAmpicillin CephalosporinsCephalosporins GentamycinGentamycin
Management of PROMManagement of PROM
2.2. PROM at termPROM at term Goal: deliver before chorioamnionitisGoal: deliver before chorioamnionitis
a.a. Expectant managementExpectant management
b.b. Induction of labor immediatelyInduction of labor immediately
Management of Term PROMManagement of Term PROM
Expectant managementExpectant managementa.a. Await spontaneous laborAwait spontaneous labor
b.b. Avoid digital cervical examination until Avoid digital cervical examination until patient in laborpatient in labor
c.c. Electronic fetal heart monitoringElectronic fetal heart monitoring
d.d. Serial monitoring for chorioamnionitisSerial monitoring for chorioamnionitis
e.e. Deliver ASAP if (+) chorioamnionitisDeliver ASAP if (+) chorioamnionitis
Management of Term PROMManagement of Term PROM
Labor induction immediately Labor induction immediately a.a. Induce labor with oxytocin infusion Induce labor with oxytocin infusion
Intracervical prostaglandin E2 gel for Intracervical prostaglandin E2 gel for preinduction cervical ripeningpreinduction cervical ripening
Bishop’s scoreBishop’s score
a.a. Continuous electronic fetal heart Continuous electronic fetal heart monitoringmonitoring
Management of PRETERM PROMManagement of PRETERM PROM
Prematurity Prematurity if not in labor, prolong if not in labor, prolong pregnancy for as long as no pregnancy for as long as no chorioamnionitischorioamnionitis
2 Options2 Options1.1. Expectant managementExpectant management
2.2. Tocolysis + corticosteroids followed by Tocolysis + corticosteroids followed by deliverydelivery
Management of PRETERM PROM: Management of PRETERM PROM: Expectant managementExpectant management
1.1. Prophylactic antibiotics Prophylactic antibiotics Decreases maternal and fetal infections Decreases maternal and fetal infections Increases latency period by 5-7 daysIncreases latency period by 5-7 days
1.1. Bed restBed rest
2.2. Avoid digital cervical exam until laborAvoid digital cervical exam until labor
3.3. Fetal well-being studiesFetal well-being studies
4.4. Serial monitoring for chorioamnionitisSerial monitoring for chorioamnionitis
5.5. Test for fetal lung maturity if Test for fetal lung maturity if >>32 32 weeksweeks
Management of PRETERM PROM: Management of PRETERM PROM: Tocolysis + corticosteroids followed by Tocolysis + corticosteroids followed by
deliverydelivery
1.1. Corticosteroid therapy Corticosteroid therapy Maximum effect 24 hours after Maximum effect 24 hours after
administrationadministration
1.1. TocolysisTocolysis Continued for 48 hrs after steroidsContinued for 48 hrs after steroids
1.1. Expectant management or induce Expectant management or induce laborlabor
Management of PREVIABLE PROMManagement of PREVIABLE PROM
PROM <25 weeksPROM <25 weeks 25-40% chance of achieving viable 25-40% chance of achieving viable
fetusfetus Risk of chorioamnionitis: 40%Risk of chorioamnionitis: 40% Fetal deformitiesFetal deformities Counseling for coupleCounseling for couple 2 Options2 Options
1.1. Expectant managementExpectant management2.2. Termination of pregnancyTermination of pregnancy
MULTIFETAL MULTIFETAL PREGNANCYPREGNANCY
ETIOLOGYETIOLOGY
Monozygotic twins arise from a single Monozygotic twins arise from a single fertilized ovum that subsequently divides fertilized ovum that subsequently divides into two similar structures, each with into two similar structures, each with potential for developing into a separate potential for developing into a separate individual (single-ovum, monozygotic or individual (single-ovum, monozygotic or identical twins).identical twins).
Dizygotic twins result from fertilization of Dizygotic twins result from fertilization of two separate ova (double-ovum, dizygotic two separate ova (double-ovum, dizygotic or fraternal twins).or fraternal twins).
1. Monozygotic 1. Monozygotic twinstwins
2. Dizygotic 2. Dizygotic twinstwins
3. 3. Chimerism - Chimerism - in an in an
individual individual whose cells whose cells
originated originated from more from more
than one than one fertilized fertilized
ovum.ovum.
ETIOLOGYETIOLOGY
Superfetation when an interval as Superfetation when an interval as long as or longer than an ovulatory long as or longer than an ovulatory cycle intervenes between cycle intervenes between fertilizations. fertilizations.
Superfecundation refers to the Superfecundation refers to the fertilization of two ova within a short fertilization of two ova within a short period of time but not at the same period of time but not at the same coitus, nor necessarily by sperm from coitus, nor necessarily by sperm from the same male.the same male.
ETIOLOGY OF MULTIFETAL PREGNANCYETIOLOGY OF MULTIFETAL PREGNANCY
RISK FACTORS FOR RISK FACTORS FOR TWINNNGTWINNNG
1.1. Race Race
2.2. Heredity – maternal family history > Heredity – maternal family history >
paternal paternal
3.3. Maternal age – peak at age 37, when Maternal age – peak at age 37, when
maximum hormonal stimulation maximum hormonal stimulation
increases rate of double ovulationincreases rate of double ovulation
4.4. Parity – fertility and multiparity (~7) Parity – fertility and multiparity (~7)
RISK FACTORS FOR RISK FACTORS FOR TWINNNGTWINNNG
5.5. Nutritional factors Nutritional factors
6.6. Pituitary gonadotropin – common Pituitary gonadotropin – common
factor linking race, age, weight, and factor linking race, age, weight, and
fertility to multiple gestation.fertility to multiple gestation.
7.7. Infertility therapy – induction of Infertility therapy – induction of
ovulation by use of gonadotropins ovulation by use of gonadotropins
(FSH plus HCG) or clomiphene. (FSH plus HCG) or clomiphene.
DIAGNOSIS: History and DIAGNOSIS: History and PEPE
1.1. History History identification of risk factors identification of risk factors
1.1. Physical examinationPhysical examination Fundic height larger than expected for Fundic height larger than expected for
gestational agegestational age
Multiplicity of fetal parts by palpationMultiplicity of fetal parts by palpation
Two distinct fetal heart tonesTwo distinct fetal heart tones
DIAGNOSIS: 3. UltrasoundDIAGNOSIS: 3. Ultrasound
Presence of 2 Presence of 2 separate placental separate placental sites and a thick sites and a thick dividing membrane dividing membrane that generally is 2 that generally is 2 mm or greater mm or greater supports supports dichorionicity.dichorionicity.
DIAGNOSIS: UltrasoundDIAGNOSIS: Ultrasound
““Twin peak” sign – Twin peak” sign – triangular projection of triangular projection of placental tissue extending placental tissue extending beyond the chorionic beyond the chorionic surface between the surface between the layers of the dividing layers of the dividing membrane seen in fused membrane seen in fused placentaplacenta
DIAGNOSISDIAGNOSIS
4.4. Biochemical test: Biochemical test: Human chorionic Human chorionic gonadotropingonadotropin in plasma and urine in plasma and urine are higher than those in singleton are higher than those in singleton pregnanciespregnancies
5.5. Radiograph of the maternal abdomen Radiograph of the maternal abdomen demonstrates multiple fetuses, demonstrates multiple fetuses, helpful in rare circumstances helpful in rare circumstances
Maternal Adaptations to Multifetal Maternal Adaptations to Multifetal PregnancyPregnancy
1.1. Nausea and vomiting - > in Nausea and vomiting - > in singleton pregnancy singleton pregnancy
2.2. Blood volume expansionBlood volume expansion 50-60% with twins 50-60% with twins vsvs 40-50% with 40-50% with
singletons singletons more pronounced more pronounced “physiologic anemia”“physiologic anemia”
Maternal Adaptations to Multifetal Maternal Adaptations to Multifetal PregnancyPregnancy
3.3. Cardiac output – increased due to Cardiac output – increased due to increased heart rate and stroke increased heart rate and stroke volumevolume
4.4. Uterus – larger size (volume of 10L, Uterus – larger size (volume of 10L, weight of 20 lbs)weight of 20 lbs)
OUTCOMES OF MULTIFETAL OUTCOMES OF MULTIFETAL PREGNANCYPREGNANCY
1.1. Spontaneous abortion more Spontaneous abortion more common in monozygotic twins.common in monozygotic twins.
2.2. Malformations Malformations Defects from twinning itself Defects from twinning itself Defects from vascular interchange Defects from vascular interchange Defects due to crowdingDefects due to crowding
Defect from twinning: Conjoined Defect from twinning: Conjoined twinstwins
Defect from Defect from twinning:twinning:
SIRENOMELIASIRENOMELIA
Persistence of Persistence of vitelline artery vitelline artery abnormal aortic abnormal aortic development development blood blood flow to lower flow to lower extremities curtailedextremities curtailed
Defect from twinning: Defect from twinning: HoloprosencephalyHoloprosencephaly
Failure of brain to Failure of brain to divide into divide into hemispheres.hemispheres.
Always accompanied Always accompanied by midline defects by midline defects e.g. cleft lip and e.g. cleft lip and palate, fused eye palate, fused eye sockets, deformities sockets, deformities of limb, heart, GIT, of limb, heart, GIT, internal organsinternal organs
Defect from twinning: Neural tube Defect from twinning: Neural tube defectdefect
Defect from twinning: Neural tube Defect from twinning: Neural tube defectdefect
ExencephalyExencephaly
Folic acid in the prevention of Folic acid in the prevention of NTDsNTDs
b. Defects from vascular interchange: b. Defects from vascular interchange: ACARDIAACARDIA
Defects from vascular interchange: Defects from vascular interchange:
MicrocephalyMicrocephaly
Defects from vascular Defects from vascular interchange:interchange:
INTESTINAL INTESTINAL ATRESIA ATRESIA
Defects from vascular interchange:Defects from vascular interchange:
APLASIA CUTIS APLASIA CUTIS
c. Defect from crowding: Talipesc. Defect from crowding: Talipes
OUTCOMES OF MULTIFETAL OUTCOMES OF MULTIFETAL PREGNANCYPREGNANCY
3.3. Low birthweightLow birthweight From restricted fetal growth and preterm deliveryFrom restricted fetal growth and preterm delivery Degree of growth restriction related to monozygosity Degree of growth restriction related to monozygosity
and number of twinsand number of twins Monozygotic twins more likely to be discordant in Monozygotic twins more likely to be discordant in
size.size.
OUTCOMES OF MULTIFETAL OUTCOMES OF MULTIFETAL PREGNANCYPREGNANCY
4.4. Preterm birthPreterm birth Duration of Duration of
gestation decreases gestation decreases as the number of as the number of fetuses increases. fetuses increases.
Major reason for the Major reason for the increased risk of increased risk of neonatal death and neonatal death and morbidity in twins.morbidity in twins.
OUTCOMES OF MULTIFETAL OUTCOMES OF MULTIFETAL PREGNANCYPREGNANCY
5.5. Prolonged pregnancyProlonged pregnancy fetal growth restriction and associated fetal growth restriction and associated
morbidity increases significantly in twins morbidity increases significantly in twins delivered at 39-41 weeks compared with delivered at 39-41 weeks compared with delivery at 38 weeks or less.delivery at 38 weeks or less.
5.5. Long-term postnatal developmentLong-term postnatal development twinning may result to delayed twinning may result to delayed
developmental milestones. developmental milestones. in discordant twins, pattern of in discordant twins, pattern of
development appears to be better in the development appears to be better in the twin who weighed more at birth. twin who weighed more at birth.
OUTCOMES OF MULTIFETAL OUTCOMES OF MULTIFETAL PREGNANCYPREGNANCY
7.7. Conjoined twinsConjoined twins twinning initiated after the embryonic twinning initiated after the embryonic
disc and rudimentary amnionic sac disc and rudimentary amnionic sac have formed and if the division of the have formed and if the division of the embryonic disc is incompleteembryonic disc is incomplete
commonly shared body site: commonly shared body site: anterior (thoracopagus)anterior (thoracopagus) posterior (pyopagus)posterior (pyopagus) cephalic (craniopagus)cephalic (craniopagus) caudal (ischiopagus)caudal (ischiopagus)
Conjoined twinsConjoined twins
THORACOPAGUS
PYGOPAGUS
CRANIOPAGUS
OUTCOMES OF MULTIFETAL OUTCOMES OF MULTIFETAL PREGNANCYPREGNANCY
8.8. Monoamnionic twins – intertwining of Monoamnionic twins – intertwining of umbilical cordsumbilical cords
9.9. Vascular communication between Vascular communication between fetusesfetuses
most vascular communications are most vascular communications are hemodynamically balanced and of little hemodynamically balanced and of little fetal consequencefetal consequence
ie. artery-to-artery, vein-to-vein, or ie. artery-to-artery, vein-to-vein, or artery-to-veinartery-to-vein
OUTCOMES OF MULTIFETAL OUTCOMES OF MULTIFETAL PREGNANCYPREGNANCY
a)a) Acardiac twin – TRAP (Twin reversed-Acardiac twin – TRAP (Twin reversed-arterial-perfusion) sequence arterial-perfusion) sequence
complication of monochorionic, complication of monochorionic, monozygotic multiple gestationmonozygotic multiple gestation
normally formed donor twin with normally formed donor twin with features of heart failurefeatures of heart failure
Recipient twin recipient twin without a Recipient twin recipient twin without a normal heart (acardius) and missing normal heart (acardius) and missing other structures, ie. other structures, ie. acephalus acephalus
B. Defects from B. Defects from vascular vascular
interchange:interchange:
ACARDIAACARDIA
OUTCOMES OF MULTIFETAL OUTCOMES OF MULTIFETAL PREGNANCYPREGNANCY
b)b) Twin-to-twin Twin-to-twin transfusion transfusion syndromesyndrome
Blood from donor Blood from donor twin to recipient twintwin to recipient twin
donor develops donor develops anemia and IUGRanemia and IUGR
recipient has recipient has polycythemia with polycythemia with circulatory overload circulatory overload hydropshydrops
donor twin is pale, donor twin is pale, recipient is plethoric recipient is plethoric
Twin-to-twin transfusion Twin-to-twin transfusion syndromesyndrome
Same sex fetusesSame sex fetuses Monochorionicity with Monochorionicity with
placental vascular placental vascular connectionsconnections
Intertwin weight Intertwin weight difference >20%difference >20%
Hydramnios in the large Hydramnios in the large twin, oligohydramnios or twin, oligohydramnios or stuck twin (in donor sac) stuck twin (in donor sac)
Hemoglobin difference >5 Hemoglobin difference >5 g/dLg/dL
Diagnosed Diagnosed postnatally: postnatally: weight weight
discordance of discordance of 15 or 20% 15 or 20%
Hgb difference Hgb difference >> 5 g/dL with the 5 g/dL with the smaller twin smaller twin being anemic being anemic
ANTENATALPOSTNATAL
OUTCOMES OF MULTIFETAL OUTCOMES OF MULTIFETAL PREGNANCYPREGNANCY
10.10. Discordant twin Discordant twin unequal size of twin unequal size of twin
fetuses fetuses sign of sign of pathological growth pathological growth restriction in one restriction in one fetusfetus
defined using larger defined using larger twin as the indextwin as the index
direct proportional direct proportional increase in perinatal increase in perinatal mortality as weight mortality as weight difference within difference within twin increasestwin increases
OUTCOMES OF MULTIFETAL OUTCOMES OF MULTIFETAL PREGNANCYPREGNANCY
13.13. Death of one (or two) twin(s) Death of one (or two) twin(s) maternal risk and prognosis for the surviving twin maternal risk and prognosis for the surviving twin
depend on the gestational age the time of the depend on the gestational age the time of the demise, the chorionicity, and time interval between demise, the chorionicity, and time interval between demise and delivery of surviving twindemise and delivery of surviving twin
FETUS PAPYRACEOUS
OUTCOMES OF MULTIFETAL OUTCOMES OF MULTIFETAL PREGNANCYPREGNANCY
14.14. Complete hydatidiform Complete hydatidiform mole and coexisting mole and coexisting fetus fetus
Two separate Two separate conceptuses: a normal conceptuses: a normal placenta in one twin and placenta in one twin and a complete molar a complete molar gestation in the othergestation in the other
Management is Management is uncertainuncertain
MANAGEMENT OF MULTIFETAL MANAGEMENT OF MULTIFETAL PREGNANCYPREGNANCY1. Antenatal1. Antenatal
Dietary requirements for calories, Dietary requirements for calories, proteins, minerals, vitamins and proteins, minerals, vitamins and essential fatty acids are increased. essential fatty acids are increased.
Hypertension Hypertension Prevention of preterm labor and Prevention of preterm labor and
delivery:delivery: bed restbed rest tocolytic therapytocolytic therapy prophylactic cervical cerclage.prophylactic cervical cerclage.
MANAGEMENT OF MULTIFETAL MANAGEMENT OF MULTIFETAL PREGNANCYPREGNANCY
2. Labor and delivery2. Labor and delivery Fetal presentation and positionFetal presentation and position
cephalic-cephalic, cephalic-breech, and cephalic-cephalic, cephalic-breech, and cephalic-transversecephalic-transverse
Conduct of labor and delivery:Conduct of labor and delivery: preterm labor,preterm labor, uterine dysfunction,uterine dysfunction, abnormal presentationsabnormal presentations prolapse of the umbilical cordprolapse of the umbilical cord premature separation of the placentapremature separation of the placenta immediate postpartum hemorrhageimmediate postpartum hemorrhage
MANAGEMENT OF MULTIFETAL MANAGEMENT OF MULTIFETAL PREGNANCYPREGNANCY
2. Labor and delivery2. Labor and delivery
Route of delivery by fetal presentation:Route of delivery by fetal presentation: Cephalic-cephalic – vaginalCephalic-cephalic – vaginal Cephalic-noncephalic – controversialCephalic-noncephalic – controversial Breech or transverse first of twin – abdominal Breech or transverse first of twin – abdominal
Anesthesia: epiduralAnesthesia: epidural
provides pain reliefprovides pain relief skeletal muscle relaxation required for skeletal muscle relaxation required for
internal podalic versioninternal podalic version rapidly extended cephalad if CS required rapidly extended cephalad if CS required
Postterm PregnancyPostterm Pregnancy
Postterm PregnancyPostterm Pregnancy
Postterm pregnancy – Postterm pregnancy – >>42 42 completed weeks (294 days) from completed weeks (294 days) from LMP LMP
Postmaturity – infant clinical features Postmaturity – infant clinical features indicating a pathologically prolonged indicating a pathologically prolonged pregnancypregnancy
PathophysiologyPathophysiology
Postmaturity syndrome – postmature Postmaturity syndrome – postmature infant with characteristic infant with characteristic appearance:appearance: wrinkled, patchy peeling skin,wrinkled, patchy peeling skin, long, thin body suggesting wastinglong, thin body suggesting wasting advanced maturity: open-eyed, advanced maturity: open-eyed,
unusually alert, old and worried-lookingunusually alert, old and worried-looking attributed to placental senescenceattributed to placental senescence
PathophysiologyPathophysiology
OligohydramniosOligohydramnios due to decreased amniotic fluid volumedue to decreased amniotic fluid volume
Fetal distressFetal distress consequence of cord compression associated consequence of cord compression associated
with oligohydramnios with oligohydramnios Fetal release of meconium in reduced Fetal release of meconium in reduced
amniotic fluid thick, viscous meconiumamniotic fluid thick, viscous meconium thick, viscous meconiumthick, viscous meconium
Fetal growth restriction in 1/3 of casesFetal growth restriction in 1/3 of cases
ManagementManagement
Antenatal surveillanceAntenatal surveillance Nonstress tests, amniotic fluid Nonstress tests, amniotic fluid
determinationsdeterminations
Cervical ripeningCervical ripening Prostaglandin gels Prostaglandin gels
Induction of laborInduction of labor Use of oxytocin Use of oxytocin
Inappropriate fetal growthInappropriate fetal growth
Baby too smallBaby too small
Baby too bigBaby too big
3 PHASES OF FETAL 3 PHASES OF FETAL GROWTHGROWTH
1.1. 1st 16 weeks gestation 1st 16 weeks gestation hyperplasiahyperplasia
5 gram/day5 gram/day
1.1. 16-32 weeks 16-32 weeks hyperplasia and hyperplasia and hypertrophyhypertrophy
15-20 g/day15-20 g/day
1.1. >32 weeks >32 weeks hypertrophy with hypertrophy with fetal fat and glycogen deposition fetal fat and glycogen deposition
30-35 g/day30-35 g/day
Factors that influence fetal growthFactors that influence fetal growth
1.1. GeneticsGenetics
2.2. HormonesHormones Insulin – somatic growth and adiposityInsulin – somatic growth and adiposity Insulin-like growth factors (IGF-I, IGF-II) – Insulin-like growth factors (IGF-I, IGF-II) –
cell division and differentiationcell division and differentiation Leptin – correlates with birthweight, Leptin – correlates with birthweight,
synthesized in adipose tissuesynthesized in adipose tissue
1.1. NutritionNutrition Maternal glucose: excessive glycemia Maternal glucose: excessive glycemia
causes macrosomia; decreased glycemia causes macrosomia; decreased glycemia causes growth restrictioncauses growth restriction
FETAL GROWTH FETAL GROWTH RESTRICTIONRESTRICTION
Small for gestational ageSmall for gestational age Birthweight <10th percentile for Birthweight <10th percentile for
gestational agegestational age
At risk for fetal deathAt risk for fetal death 0.2% for normal 38 weekers vs 2% for SGAs0.2% for normal 38 weekers vs 2% for SGAs
Uteroplacental isufficiencyUteroplacental isufficiency
Complications of SGA Complications of SGA babiesbabies
Fetal demiseFetal demise AsphyxiaAsphyxia Meconium aspirationMeconium aspiration Neonatal hypoglycemiaNeonatal hypoglycemia HypothermiaHypothermia Abnormal neurological developmentAbnormal neurological development
Symmetrical FGRSymmetrical FGR
Head to abdomen circumference ratio (HC/AC) Head to abdomen circumference ratio (HC/AC) Ratio >95% percentileRatio >95% percentile
Asymmetric fetus had bigger brain, protected from full Asymmetric fetus had bigger brain, protected from full effects of growth retarding stimulus.effects of growth retarding stimulus.
Preferential shunting of oxygen and nutrients to brain Preferential shunting of oxygen and nutrients to brain
Early insult from viral infection, chemical Early insult from viral infection, chemical exposure, aneuploidy affecting cellular number exposure, aneuploidy affecting cellular number an sizean size
Severe preeclampsia, fetal distress, operative Severe preeclampsia, fetal distress, operative intervention, low apgar scoreintervention, low apgar score
Asymmetrical FGR Asymmetrical FGR
Late insult: uteroplacental Late insult: uteroplacental insufficiency affecting cell sizeinsufficiency affecting cell size
HypertensionHypertension
Risk factorsRisk factors
1.1. Constitutionally small mothersConstitutionally small mothers Mother <100 lbs with two-fold increase Mother <100 lbs with two-fold increase
in risk for SGAin risk for SGA
1.1. Poor maternal weight gain and Poor maternal weight gain and nutritionnutrition
Weight gain during pregnancyWeight gain during pregnancy
1.1. Social deprivationSocial deprivation Lifestyle and use of illicit substances, Lifestyle and use of illicit substances,
alcohol, smoking, nutrition alcohol, smoking, nutrition
Risk factorsRisk factors
4.4. Fetal infectionsFetal infectionsa.a. Cytomegalovirus – direct cytolysis and loss of Cytomegalovirus – direct cytolysis and loss of
functional cellsfunctional cellsb.b. Rubella – vascular insufficiency endothelial Rubella – vascular insufficiency endothelial
cell damage, decreased rate of cell division cell damage, decreased rate of cell division c.c. Hepatitis A and BHepatitis A and Bd.d. ListeriosisListeriosise.e. TuberculosisTuberculosisf.f. Syphilis –megaplacenta due to edema and Syphilis –megaplacenta due to edema and
perivascular inflammationperivascular inflammationg.g. ToxoplasmosisToxoplasmosish.h. Congenital malariaCongenital malaria
Risk factorsRisk factors
5.5. Chromosomal abnormalitiesChromosomal abnormalities Autosomal trisomies (21, 18, 13, 16) – Autosomal trisomies (21, 18, 13, 16) –
reduced number of small arteries in tertiary reduced number of small arteries in tertiary villi villi uteroplacental insufficiency and uteroplacental insufficiency and abnormal cell growth and differentiationabnormal cell growth and differentiation
5.5. Congenital malformationsCongenital malformations
6.6. Primary disorders of bone and cartilage Primary disorders of bone and cartilage
Risk factorsRisk factors
8.8. Chemical teratogensChemical teratogens Anticonvulsants: phenytoin and Anticonvulsants: phenytoin and
trimethadionetrimethadione NarcoticsNarcotics SmokingSmoking AlcoholAlcohol CocaineCocaine
Risk factorsRisk factors
9.9. Vascular diseaseVascular disease
10.10. Chronic renal diseaseChronic renal disease
11.11. Chronic hypoxiaChronic hypoxia
12.12. Maternal anemiaMaternal anemia
13.13. Placental and cord abnormalitiesPlacental and cord abnormalities Chronic placental separationChronic placental separation InfarctionInfarction ChorioangiomaChorioangioma
Risk factorsRisk factors
14.14. Multiple gestationMultiple gestation
15.15. APAS – vascular thrombosis; APAS – vascular thrombosis; maternal platelet aggregation and maternal platelet aggregation and placental thrombosisplacental thrombosis
Anticardiolipin antibodyAnticardiolipin antibody Lupus anticoagulantLupus anticoagulant
14.14. Extrauterine pregnancyExtrauterine pregnancy
SCREENING AND DIAGNOSISSCREENING AND DIAGNOSIS
1.1. Establish gestational ageEstablish gestational age
2.2. Maternal weight gainMaternal weight gain
3.3. Uterine fundal growthUterine fundal growth Normal: 18-30 weeks, fundic height in cm = Normal: 18-30 weeks, fundic height in cm =
gestation in weeks +1 cmgestation in weeks +1 cm
4.4. Identify risk factorsIdentify risk factors history of growth retarded fetushistory of growth retarded fetus
SCREENING AND DIAGNOSISSCREENING AND DIAGNOSIS
5.5. Serial sonographic measurements of Serial sonographic measurements of head, abdominal, femoralhead, abdominal, femoral
Abdominal circumference is most reliableAbdominal circumference is most reliable
5.5. Doppler velocimetry Doppler velocimetry Umbilical artery – absent or reversed flow Umbilical artery – absent or reversed flow
increased impedance increased impedance IUGR IUGR Adjunct to NST and BPPAdjunct to NST and BPP
Management of Growth Restricted Management of Growth Restricted FetusFetus
Look for congenital malformationsLook for congenital malformations
Determine if fetus is in poor Determine if fetus is in poor conditioncondition
Cordocentesis for karyotypingCordocentesis for karyotyping Lethal aneupliody Lethal aneupliody
Weigh risk of fetal death vs preterm Weigh risk of fetal death vs preterm deliverydelivery
FGR near TERMFGR near TERM
1.1. Prompt delivery: Prompt delivery: >>34 weeks34 weeks Reassuring FHR pattern: vaginal Reassuring FHR pattern: vaginal
deliverydelivery Fetal distress: CSFetal distress: CS
2.2. Expectant managementExpectant management Fetal well being studiesFetal well being studies
FGR remote from TERMFGR remote from TERM
1.1. <34 weeks + normohydramnios + <34 weeks + normohydramnios + normal fetal surveillancenormal fetal surveillance
Observation Observation Fetal surveillance every 2-3 weeks Fetal surveillance every 2-3 weeks Amniocentesis for fetal lung maturity Amniocentesis for fetal lung maturity
1.1. With fetal growth With fetal growth allow allow pregnancy to continuepregnancy to continue
2.2. Fetal compromise Fetal compromise Deliver Deliver
FGR remote from TERMFGR remote from TERM
Bed rest, LLD positionBed rest, LLD position Nutritional supplementationNutritional supplementation HydrationHydration Oxygen therapyOxygen therapy MedicationsMedications
Antihypertensive drugsAntihypertensive drugs AspirinAspirin HeparinHeparin DipyridamoleDipyridamole Nitrol patchNitrol patch
Labor and Delivery of Growth- Labor and Delivery of Growth- restricted Fetusrestricted Fetus
Continuous fetal heart rate pattern Continuous fetal heart rate pattern surveillancesurveillance Uteroplacental insufficiencyUteroplacental insufficiency Oligohydramnios Oligohydramnios cord compression cord compression
Meconium aspiration Meconium aspiration HypothermiaHypothermia Polycythemia and hyperviscosityPolycythemia and hyperviscosity HypoglycemiaHypoglycemia
DISEASES and INJURIES of DISEASES and INJURIES of the FETUS and the the FETUS and the
NEWBORNNEWBORN
HYALINE MEMBRANE DISEASEHYALINE MEMBRANE DISEASE
Etiology: inadequate surfactant Etiology: inadequate surfactant production by type II pneumonocytesproduction by type II pneumonocytes
Signs and symptomsSigns and symptoms tachypnea and chest wall retractiontachypnea and chest wall retraction
expiration is accompanied by a whimper expiration is accompanied by a whimper and grunt (combination of “grunting and and grunt (combination of “grunting and flaringflaring
HYALINE MEMBRANE DISEASEHYALINE MEMBRANE DISEASE
chest x-ray: chest x-ray: diffuse diffuse reticulogranulareticulogranular infiltrate with r infiltrate with an air-filled an air-filled tracheobronchitracheobronchial tree (air al tree (air bronchogram)bronchogram)
HYALINE MEMBRANE DISEASEHYALINE MEMBRANE DISEASE
Complications Complications bronchopulmonary dysplasiabronchopulmonary dysplasia pulmonary hypertension pulmonary hypertension retinopathy of prematurityretinopathy of prematurity
HYALINE MEMBRANE DISEASEHYALINE MEMBRANE DISEASE Continuous positive Continuous positive
airway pressure airway pressure (CPAP) prevents (CPAP) prevents collapse of collapse of unstable alveoliunstable alveoli
Surfactant Surfactant prophylaxis of prophylaxis of
preterm infants at preterm infants at risk for RDSrisk for RDS
Rescue for those Rescue for those with established with established diseasedisease
RETINOPATHY OF PREMATURITYRETINOPATHY OF PREMATURITY
Retinal vessels Retinal vessels damaged by damaged by excessive oxygenexcessive oxygen
Oxygen induces Oxygen induces severe severe vasoconstriction, vasoconstriction, endothelial endothelial damage and damage and vessel obliterationvessel obliteration
MECONIUM ASPIRATIONMECONIUM ASPIRATION
Peripartum inhalation of meconium-stained Peripartum inhalation of meconium-stained amniotic fluid amniotic fluid inflammation of inflammation of pulmonary tissues and hypoxiapulmonary tissues and hypoxia
May progress to persistent pulmonary May progress to persistent pulmonary hypertension, morbidity and deathhypertension, morbidity and death
Pregnancies at risk for meconium Pregnancies at risk for meconium aspirationaspiration OligohydramniosOligohydramnios Cord compression Cord compression Uteroplacental insufficiencyUteroplacental insufficiency
MECONIUM ASPIRATIONMECONIUM ASPIRATION
Chest X rayChest X ray
MECONIUM ASPIRATIONMECONIUM ASPIRATION
Prevention Prevention Suction infant’s Suction infant’s
mouth and nares mouth and nares before shoulders are before shoulders are delivereddelivered
Suction under direct Suction under direct visualization as soon visualization as soon as infant who has as infant who has passed thick, passed thick, particulate meconium particulate meconium is placed on radiant is placed on radiant warmerwarmer
INTRAVENTRICULAR INTRAVENTRICULAR HEMORRHAGEHEMORRHAGE
Etiology Etiology Subdural hematoma – traumaSubdural hematoma – trauma Subarachnoid and intracerebellar Subarachnoid and intracerebellar
hemorrhage – trauma in term infants, hemorrhage – trauma in term infants, hypoxia in preterm infantshypoxia in preterm infants
Periventricular-intraventricular hemorrhage Periventricular-intraventricular hemorrhage Unknown cause in 25% of casesUnknown cause in 25% of cases
INTRAVENTRICULAR INTRAVENTRICULAR HEMORRHAGEHEMORRHAGE
INTRAVENTRICULAR INTRAVENTRICULAR HEMORRHAGEHEMORRHAGE
Patholophysiology: damage to the germinal Patholophysiology: damage to the germinal matrix capillary network matrix capillary network extravasation of extravasation of blood into the surrounding tissues blood into the surrounding tissues capillary network is fragile in preterm infantscapillary network is fragile in preterm infants
Long term sequelaeLong term sequelae Periventricular leukomalaciaPeriventricular leukomalacia Neurodevelopmental handicapsNeurodevelopmental handicaps
Treatment: corticosteroids before delivery Treatment: corticosteroids before delivery appears to prevent intraventricular appears to prevent intraventricular hemorrhage in preterm infantshemorrhage in preterm infants
CEREBRAL PALSYCEREBRAL PALSY Nonprogressive motor Nonprogressive motor
disorder of early infancy disorder of early infancy involving involving >> 1 limbs 1 limbs resulting from muscular resulting from muscular spasticity or paralysisspasticity or paralysis
Types Types Spastic quadriplegiaSpastic quadriplegia DiplegiaDiplegia HemiplegiaHemiplegia Choreoathetoid typeChoreoathetoid type Mixed varietiesMixed varieties
CEREBRAL PALSYCEREBRAL PALSY Risk factorsRisk factors
1.1. Genetic abnormalities such Genetic abnormalities such as maternal mental as maternal mental retardation, microcephaly, retardation, microcephaly, congenital malformationscongenital malformations
2.2. Birthweight l< 2000 gramsBirthweight l< 2000 grams
3.3. Gestational age <32 weeksGestational age <32 weeks
4.4. Infection Infection
Correlation with Correlation with intrapartum asphyxia intrapartum asphyxia controversialcontroversial
NEONATAL ENCEPHALOPATHYNEONATAL ENCEPHALOPATHY
Syndrome of disturbed neurological Syndrome of disturbed neurological function in the earliest days of life in term function in the earliest days of life in term infantinfant
Consists of difficulty in initiating and Consists of difficulty in initiating and maintaining respiration, depressed tone maintaining respiration, depressed tone and reflexes, subnormal level of and reflexes, subnormal level of consciousness and frequently seizuresconsciousness and frequently seizures
Believed to be a consequence of an Believed to be a consequence of an hypoxic-ischemic insulthypoxic-ischemic insult
ANEMIAANEMIA
Cord hemoglobin < 14 g/dl (>35 weeks, mean Cord hemoglobin < 14 g/dl (>35 weeks, mean cord hemoglobin concentration = 17 g/dL) cord hemoglobin concentration = 17 g/dL)
Hemoglobin due to delayed cord clamping Hemoglobin due to delayed cord clamping appreciable volume of blood being expressed from appreciable volume of blood being expressed from the placenta through the cord of the infantthe placenta through the cord of the infant
Hemoglobin if placenta is cut or torn, a fetal Hemoglobin if placenta is cut or torn, a fetal vessel is perforated or lacerated, or the infant is vessel is perforated or lacerated, or the infant is held well above the level of the placenta before held well above the level of the placenta before cord clampingcord clamping
ABO INCOMPATIBILITYABO INCOMPATIBILITY
Incompatibility for the major blood Incompatibility for the major blood group antigens A and B is the most group antigens A and B is the most common cause of hemolytic disease common cause of hemolytic disease of the newbornof the newborn
Invariably causes mild disease, such Invariably causes mild disease, such as neonatal jaundice or anemia but as neonatal jaundice or anemia but not erythroblastosis fetalisnot erythroblastosis fetalis
Treatment: PhototherapyTreatment: Phototherapy
IMMUNE HYDROPSIMMUNE HYDROPS
Subcutaneous edemaSubcutaneous edema
Effusion into the Effusion into the serous cavities - serous cavities - presence of abnormal presence of abnormal fluid in fluid in >> 2 sites such 2 sites such as thorax, abdomen as thorax, abdomen or skin;or skin;
Edematous placenta, Edematous placenta, enlarged and boggyenlarged and boggy
IMMUNE HYDROPSIMMUNE HYDROPS Pathophysiology: obscurePathophysiology: obscure TheoriesTheories
Heart failure and capillary leakage from profound anemia,Heart failure and capillary leakage from profound anemia, Portal and umbilical venous hypertension from hepatic parenchymal Portal and umbilical venous hypertension from hepatic parenchymal
disruption by extramedullary hematopoiesisdisruption by extramedullary hematopoiesis Decreased colloid oncotic pressure from hypoproteinemia caused by liver Decreased colloid oncotic pressure from hypoproteinemia caused by liver
dysfunctiondysfunction
IMMUNE HYDROPSIMMUNE HYDROPS
Treatment: identify woman at risk at first Treatment: identify woman at risk at first prenatal appointmentprenatal appointment After identification of isoimmunization and the After identification of isoimmunization and the
fetus at risk for optimal outcome, subsequent fetus at risk for optimal outcome, subsequent management is individualizedmanagement is individualized
Prevention: Prevention: anti-D immunoglobulin to Rh(-) women at 28 anti-D immunoglobulin to Rh(-) women at 28
weeks, and after delivery if the infant is D-weeks, and after delivery if the infant is D-positivepositive
Immunoglobulin given to Rh(-) women after Immunoglobulin given to Rh(-) women after miscarriage, abortion, or evacuation of a molar miscarriage, abortion, or evacuation of a molar or ectopic pregnancyor ectopic pregnancy
NONIMMUNE HYDROPSNONIMMUNE HYDROPS
EtiologyEtiology cardiac abnormalitiescardiac abnormalities fetal heart failurefetal heart failure chromosomal abnormalitieschromosomal abnormalities twin-to-twin transfusion syndrometwin-to-twin transfusion syndrome severe anemiasevere anemia inborn errors of metabolisminborn errors of metabolism anomalous lymph systemanomalous lymph system
Treatment depends on the causeTreatment depends on the cause
HEMORRHAGIC DISEASE of the HEMORRHAGIC DISEASE of the NEWBORNNEWBORN
Spontaneous internal or external bleeding Spontaneous internal or external bleeding accompanied by hypoprothrombinemia & accompanied by hypoprothrombinemia & very low levels of other vitamin K-very low levels of other vitamin K-dependent coagulation factors (V, VII, IX dependent coagulation factors (V, VII, IX and X)and X)
EtiologyEtiology dietary vitamin K deficiency – main causedietary vitamin K deficiency – main cause HemophiliaHemophilia congenital syphiliscongenital syphilis SepsisSepsis thrombocytopenia purpurathrombocytopenia purpura erythroblastosis erythroblastosis intracranial hemorrhageintracranial hemorrhage
Prevention: Vit K 1 mg IM at deliveryPrevention: Vit K 1 mg IM at delivery
NECROTIZING ENTEROCOLITISNECROTIZING ENTEROCOLITIS
Clinical findings: Clinical findings: abdominal abdominal distention, ileus distention, ileus and bloody stoolsand bloody stools
Seen in low Seen in low birthweight infantsbirthweight infants
NECROTIZING ENTEROCOLITISNECROTIZING ENTEROCOLITIS
Radiologic Radiologic evidence: evidence: pneumatosis pneumatosis intestinalis caused intestinalis caused by intestinal wall by intestinal wall gas from invasion gas from invasion by gas-forming by gas-forming bacteria and bowel bacteria and bowel perforationperforation
FETAL DEATHFETAL DEATH Fetal causes (25-40%)Fetal causes (25-40%)
chromosomal chromosomal anomaliesanomalies
nonchromosomal birth nonchromosomal birth defectsdefects
nonimmune hydropsnonimmune hydrops infectionsinfections
Maternal (5-10%)Maternal (5-10%) APASAPAS DMDM Hypertension Hypertension TraumaTrauma Abnormal laborAbnormal labor SepsisSepsis Acidosis, hypoxiaAcidosis, hypoxia
Uterine ruptureUterine rupture Postterm pregnancyPostterm pregnancy DrugsDrugs
Placental causes (25-Placental causes (25-35%)35%) Abruption, previaAbruption, previa fetal-maternal fetal-maternal
hemorrhagehemorrhage cord accidentcord accident placental insufficiency, placental insufficiency,
intrapartum asphyxiaintrapartum asphyxia twin-to-twin transfusiontwin-to-twin transfusion chorioamnionitischorioamnionitis
Unexplained (25-35%)Unexplained (25-35%)
INJURIES of the FETUS and INJURIES of the FETUS and NEWBORNNEWBORN
Intracranial hemorrhageIntracranial hemorrhage Sites: subdural, subarachnoid, cortical, white Sites: subdural, subarachnoid, cortical, white
matter, cerebellar, intraventricular, and matter, cerebellar, intraventricular, and periventricularperiventricular
Most common type: IC bleed in the germinal Most common type: IC bleed in the germinal matrixmatrix
Severe molding & overlapping of parietal Severe molding & overlapping of parietal bones, bridging veins from the cerebral bones, bridging veins from the cerebral cortex to the sagittal sinus may tearcortex to the sagittal sinus may tear
Causes Causes Birth trauma during difficult labor and delivery Birth trauma during difficult labor and delivery Prenatal factors: genetic and environmentalPrenatal factors: genetic and environmental
CEPHALHEMATOMACEPHALHEMATOMA
Injury to periosteum Injury to periosteum of the skull during of the skull during labor and deliverylabor and delivery
Periosteal limitations, Periosteal limitations, definite palpable definite palpable edgesedges
May not appear for May not appear for hours after delivery, hours after delivery, often growing larger often growing larger and disappearing and disappearing only after weeks or only after weeks or even monthseven months
CAPUT SUCCEDANEUMCAPUT SUCCEDANEUM Focal swelling of the Focal swelling of the
scalp from edema that scalp from edema that overlies the periosteumoverlies the periosteum
Maximal at birth, then Maximal at birth, then grows smallergrows smaller
Usually disappears Usually disappears within a few hours if within a few hours if small, and within a few small, and within a few days if very largedays if very large
CAPUT SUCCEDANEUM vs CAPUT SUCCEDANEUM vs CEPHALHEMATOMACEPHALHEMATOMA
CAPUT SUCCEDANEUM CEPHALHEMATOMA
NERVE INJURIESNERVE INJURIES
Spinal injury – Spinal injury – overstretching the overstretching the spinal cord and spinal cord and associated associated hemorrhage hemorrhage following excessive following excessive traction during a traction during a breech deliverybreech delivery
NERVE INJURIESNERVE INJURIES
Brachial plexus Brachial plexus injury – Duchenne injury – Duchenne paralysis results paralysis results from stretching or from stretching or tearing of the upper tearing of the upper roots of the brachial roots of the brachial plexusplexus
NERVE INJURIESNERVE INJURIES
Facial paralysis – Facial paralysis – seen with delivery seen with delivery of an infant in of an infant in which head has which head has been seized been seized obliquely with obliquely with forcepsforceps
FRACTURESFRACTURES
Fractures Fractures ClavicularClavicular HumeralHumeral FemoralFemoral Skull fracturesSkull fractures
CONGENITAL MALFORMATIONS CONGENITAL MALFORMATIONS AND INHERITED DISEASESAND INHERITED DISEASES
Women at risk for fetal aneuploidyWomen at risk for fetal aneuploidy
1.1. Women with singleton pregnancy at least Women with singleton pregnancy at least age 35 at deliveryage 35 at delivery
2.2. Women with dizygotic twin pregnancy at Women with dizygotic twin pregnancy at least age 31 at deliveryleast age 31 at delivery
Risk for fetal Down syndrome – 1:190Risk for fetal Down syndrome – 1:190
1.1. Previous pregnancy with autosomal trisomyPrevious pregnancy with autosomal trisomy 1% occurrence, until age-related risk >1.1% occurrence, until age-related risk >1.
1.1. Previous pregnancy with triple XXX (47XXX) Previous pregnancy with triple XXX (47XXX) or Klinefelter syndrome 47 XXYor Klinefelter syndrome 47 XXY
Extra X may be maternal or paternalExtra X may be maternal or paternal 47 XYY and 45 X not at high risk for recurrence47 XYY and 45 X not at high risk for recurrence
Women at risk for fetal aneuploidyWomen at risk for fetal aneuploidy
5.5. Woman or partner who is a translocation Woman or partner who is a translocation carrier.carrier.
5 – 30% risk5 – 30% risk
5.5. Woman or partner who is a chromosomal Woman or partner who is a chromosomal inversion carrier.inversion carrier.
5 – 10% risk5 – 10% risk
5.5. History of triploidyHistory of triploidy Recurrence risk is 1 – 1.5% if fetus survives 1Recurrence risk is 1 – 1.5% if fetus survives 1stst
trimestertrimester
Women at risk for fetal aneuploidyWomen at risk for fetal aneuploidy
8.8. Repetitive spontaneous 1Repetitive spontaneous 1stst trimester trimester losseslosses
Karyotype on the parents most usefulKaryotype on the parents most useful
9.9. Parental aneuploidyParental aneuploidy Trisomy 21, 47,XXX and 47,XYY have 30% Trisomy 21, 47,XXX and 47,XYY have 30%
risk of having trisomic offspring risk of having trisomic offspring Detect it through maternal and paternal Detect it through maternal and paternal
karyotypingkaryotyping
9.9. Fetus with major structural defect Fetus with major structural defect identified by ultrasoundidentified by ultrasound
Congenital Heart DiseaseCongenital Heart Disease
Most common birth defect, 7:1000 birthsMost common birth defect, 7:1000 births
EtiologyEtiology GeneticGenetic
Environmental – DM, viral infections, poor OB history, Environmental – DM, viral infections, poor OB history, smoking, drug usesmoking, drug use
Recurrence risk for CHD:Recurrence risk for CHD: Mother > 2 siblings > 1 sibling > father Mother > 2 siblings > 1 sibling > father
Prenatal diagnosis: fetal 2D echocardiogram at Prenatal diagnosis: fetal 2D echocardiogram at 20 – 22 weeks gestation20 – 22 weeks gestation
Congenital Heart DiseaseCongenital Heart Disease
ASDPDA
Congenital Heart DiseaseCongenital Heart Disease
TETRALOGY OF FALLOT
TRICUSPID ATRESIA
Neural Tube DefectsNeural Tube Defects
Family history of neural tube defectsFamily history of neural tube defects most important risk factormost important risk factor Risk to 1Risk to 100 relative 2-3%, related to degree of relative 2-3%, related to degree of
relations, # of relatives affected relations, # of relatives affected
Exposure to environmental agentsExposure to environmental agents Period of risky exposure: 1Period of risky exposure: 1stst 28 days gestation 28 days gestation HyperglycemiaHyperglycemia HyperthermiaHyperthermia Drugs: carbamazepine, valproic acid, Drugs: carbamazepine, valproic acid,
aminopterin, isotretinoinaminopterin, isotretinoin
Neural Tube DefectsNeural Tube Defects
NTDs as part of a genetic syndrome NTDs as part of a genetic syndrome with known recurrence riskwith known recurrence risk Inherited syndromes: Meckel-Gruber, Inherited syndromes: Meckel-Gruber,
Roberts-SC phocomeliaRoberts-SC phocomelia
Known high-risk racial, ethnic groups Known high-risk racial, ethnic groups or living in high-risk geographic areasor living in high-risk geographic areas UK – highest incidenceUK – highest incidence Sikhs in India > Sikhs in CanadaSikhs in India > Sikhs in Canada
Screening for NTDsScreening for NTDs
Maternal serum Maternal serum αα -fetoprotein-fetoprotein At 15-22 weeks gestation, At 15-22 weeks gestation, >>2.0-2.5 MOM2.0-2.5 MOM
Targeted ultrasound Targeted ultrasound Major cranial, spinal defects can be detectedMajor cranial, spinal defects can be detected
Lemon sign, banana signLemon sign, banana sign
Risk of NTD reduced by 95% if none found by Risk of NTD reduced by 95% if none found by UTZUTZ
Amniocentesis for AF Amniocentesis for AF αα FPFP NTD suspect with elevated NTD suspect with elevated αα FP but (-) UTZFP but (-) UTZ Elevated serum and AF Elevated serum and AF αα FP, do karyotyping FP, do karyotyping
Ultrasound-guided AMNIOCENTESISUltrasound-guided AMNIOCENTESIS
Neural Tube DefectsNeural Tube Defects
ANENCEPHALY
INIENCEPHALY
Neural Tube DefectsNeural Tube Defects
DOWN’S SYNDROMEDOWN’S SYNDROME
Majority of Down syndrome pregnancies Majority of Down syndrome pregnancies are de novo and in women age <35.are de novo and in women age <35.
Maternal age – most important risk factorMaternal age – most important risk factor Multiple marker screeningMultiple marker screening
Low Low α −α −fetoproteinfetoprotein Elevated Elevated β −β −human chorionic gonadotrophinhuman chorionic gonadotrophin Decreased unconjugated estriolDecreased unconjugated estriol
FRAGILE X SYNDROMEFRAGILE X SYNDROME
Most common Most common cause of familial cause of familial mental retardationmental retardation
Affected female Affected female carriers are normal.carriers are normal.
Long face, Long face, elongated ears, elongated ears, testes larger than testes larger than normal.normal.
CYSTIC FIBROSISCYSTIC FIBROSIS
Autosomal Recessive Autosomal Recessive 1:25 Euro Caucasians1:25 Euro Caucasians
Abnormal sweat Abnormal sweat chloride level, chr chloride level, chr pulmonary disease, pulmonary disease, pancreatic pancreatic insufficiency, liver insufficiency, liver disease, obstructive disease, obstructive azoospermiaazoospermia
Pregnancy Pregnancy terminationtermination
CONGENITAL DIAPHRAGMATIC HERNIACONGENITAL DIAPHRAGMATIC HERNIA
1:37001:3700 Fetal surgical Fetal surgical
correction to correction to restore normal restore normal intrathoracic intrathoracic anatomy and allow anatomy and allow pulmo dev’t pulmo dev’t prevent pulmo prevent pulmo hypoplasiahypoplasia
Management of fetuses with Management of fetuses with congenital anomaliescongenital anomalies
Team approachTeam approach
Route of deliveryRoute of delivery CS if malformation will cause dystociaCS if malformation will cause dystocia e.g. conjoined twins, hydrocephaluse.g. conjoined twins, hydrocephalus
Intrauterine fetal therapyIntrauterine fetal therapy Pulmonary immaturity – transplacental glucocorticoidsPulmonary immaturity – transplacental glucocorticoids Intrauterine growth restriction – protein-caloresIntrauterine growth restriction – protein-calores
Management of fetuses with Management of fetuses with congenital anomaliescongenital anomalies
Malformations needing Malformations needing early correction ex early correction ex uteroutero Obstructive Obstructive
hydrocephalus, hydrocephalus, hydronephrosishydronephrosis
HydropsHydrops IUGRIUGR Intestinal ischemiaIntestinal ischemia
VolvulusVolvulus Meconium ileusMeconium ileus
Malformations best Malformations best corrected in term infantcorrected in term infant GIT atresiasGIT atresias Meconium ileusMeconium ileus Small meningocoele, spina Small meningocoele, spina
bifidabifida Smal sacrococcygeal Smal sacrococcygeal
teratomateratoma Craniofacial, chest wall and Craniofacial, chest wall and
extremity deformitiesextremity deformities
OBSTETRIC OBSTETRIC COMPLICATIONSCOMPLICATIONS
Maternal and fetal Maternal and fetal conditions that conditions that make the make the pregnancy at risk pregnancy at risk for morbidity and for morbidity and mortality:mortality:
Multifetal pregnancyMultifetal pregnancy Preterm laborPreterm labor Postterm pregnancyPostterm pregnancy Inappropriate fetal Inappropriate fetal
growthgrowth
Premature rupture of Premature rupture of membranesmembranes
Congenital Congenital malformations and malformations and inherited diseasesinherited diseases
Diseases and injuries of Diseases and injuries of the fetus and the the fetus and the newborn infantnewborn infant
DefinitionDefinition Risk factorsRisk factors PathophysiologyPathophysiology ManagementManagement
hydranencephalyhydranencephaly