Fetal Complications of Pregnancy

Question 1

how do you estimate antepartum fetal weight

Answer 1

U/S

Question 2

define small for gestational age (SGA)

Answer 2

fetuses whose estimated birth weight are below the 10th percentile

describes neonates with signs of fetal growth disruption but in whom the causative factor is unknown

Question 3

define large for gestational age (LGA)

Answer 3

fetuses whose estimated birth weight is above the 90th percentile

Question 4

what are the two types of SGA

Answer 4

symmetrical –> proportionally small

asymmetrical –> certain organs are disproportionately small (head circumference is usually preferentially preserved due to brain, vs wasting of the torso and extremities)

Question 5

by term, what volume of maternal cardiac output is passing through the placental exchange network per minute

Answer 5

600 mL/min

Question 6

what determines the ultimate growth potential of the fetus

Answer 6

genetics

when the expected regulatory processes occur in the fetus, mother and placenta, normal growth ensues

Question 7

why do we care about SGA

Answer 7

associated with higher rates of mortality and morbidity for their gestational age

even within this category, those with lower percentile birth weights (5% etc) have worse outcomes –> BUT, SGA infants do better than those of same weight but that are delivered at earlier gestational ages

Question 8

what are the two causative categories of SGA

Answer 8

1. decreased growth potential

2. IUGR

Question 9

risk factors for decreased growth potential causing SGA

Answer 9

genetic and chromosomal abnormalities

intrauterine infection

teratogenic exposure

substance use

radiation exposure

small maternal stature

pregnancy at high altitudes

female fetus

Question 10

risk factors for IUGR causing SGA

Answer 10

maternal factors including:
HTN
anemia
chronic renal disease
malnutrition
severe diabetes with extensive vascular disease 
SLE
antiphospholipid antibody syndrome

placental factors including:
placenta previa
chronic abruption
placental infarction
multiple gestations

Question 11

what % of decreased growth potential SGA is caused by congenital abnormalities (i.e the trisomies)

Answer 11

10-15%

i.e Down, Patau, Edward, Turner, osteogenesis imperfecta, achondroplasia, NTDs, anancephaly and other autosomal recessive disorders

Question 12

name some intrauterine infections that can leads to decreased growth potential SGA

Answer 12

CMV

rubella

probably account for 10-15% of all SGA babies

Question 13

what are the two most common teratogens that cause decreased growth potential SGA

Answer 13

alcohol and cigarettes

Question 14

what % of babies diagnosed with decreased growth potential SGA are just constitutionally small

Answer 14

10%

based on parental stature or genetic potential

appears to vary by race/ethnicity

Question 15

what two general types of growth occur in utero, and when do they happen

Answer 15

before 20 weeks: hyperplastic–> increasing number of cells

after 20 weeks: hypertrophic–> increasing size of cells

therefore–> insult before 20 weeks more likely to cause symmetric growth restriction whereas after 20 weeks more likely to result in asymmetric growth

Question 16

what do we think causes asymmetric growth

Answer 16

decreased nutrition and oxygen being delivered across the placenta which is then shunted to the fetal brain preferentially

2/3 of the time growth restriction is asymmetric and can be identified by increased head-to-abdo measurements

Question 17

when should you get an U/S to investigate fetal growth

Answer 17

when SFH is 3 cm less than expected

note that using SFH as a marker for fetal growth has a sensitivity of only about 50%–> therefore, if risk factors exist, might consider getting U/S even without abnormal fetal measurements

should also check dating for accuracy

Question 18

how do you manage a fetus suspected of being SGA/IUGR, and how can you use U/S to distinguish the two

Answer 18

serial U/S every 2-3 weeks

a fetus with decreased growth potential will usually start small and stay small whereas one with IUGR will progressively fall off the growth curve

can also use doppler investigation of the umbilical artery–> flow during diastole should never be absent or reversed but in the setting of increased placental resistance (i.e thrombosed or calcified placenta) diastolic flow can be absent or reversed

reversed flow has high risk of IUFD

thus, those with abnormal dopplers are often delivered early, whereas those with normal dopplers are often managed expectantly

Question 19

what might cause absent or reversed diastolic flow in the umbilical artery on doppler

Answer 19

calcified or thrombosed placenta

Question 20

how are patients at risk for SGA due to placental insufficiency, preeclampsia, collagen vascular disorders or vascular disease often treated

Answer 20

with low dose aspirin

Question 21

how are patients at risk for SGA due to history of prior placental thrombosis, thrombophilias, or antiphospholipid antibody syndrome treated

Answer 21

heparin and corticosteroids as well as low dose aspirin

mixed results

Question 22

is there a reason to expedite delivery of fetuses who have been small throughout gestation

Answer 22

no

however, risk to fetus is probably lower with delivery if they have fallen off the growth curve later in gestation–> assess with NST, OCT, BPP and umbilical dopplers (if non reassuring, deliver)

Question 23

which is more important–dx of fetal macrosomia or LGA

Answer 23

fetal macrosomia–> greater risk for birth trauma or C/S

Question 24

what is the definition of fetal macrosomia

Answer 24

vary–> ACOG uses BIRTH WEIGHT ABOVE 4500 g

others use birth weights above 4000 g or 4200 g

Question 25

what are the risks associated with fetal macrosomia

Answer 25

shoulder dystocia birth trauma with resultant brachial plexus injuries with vaginal deliveries low apgar scores hypoglycemia polycytheia hypocalcemia jaundice

Question 26

what are the risks associated with LGA babies in infancy

Answer 26

childhood leukemia wilms tumour osteosarcoma

Question 27

what are the risks to mom with LGA/macrosomic fetuses

Answer 27

C/S risk higher (failure to progress) perineal trauma post partum hemorrhage

Question 28

what is the most classic risk factor for fetal macrosomia

Answer 28

preexisting or gestational diabetes mellitus

Question 29

list the risk factors for fetal macrosomia

Answer 29

diabetes maternal obesity with BMI above 30 or weight greater than 90kg increased maternal weight gain in pregnancy previous delivery of LGA infant postterm pregnancies multiparity advanced maternal age male infant beckwith-wiedemann syndrome (pancreatic islet cell hyperplasia)

Question 30

is U/S a good tool for screening for LGA infants

Answer 30

not really--PPV is only 50% for LGA infants (more useful for SGA fetuses)

Question 31

how do you manage LGA/macrosomia

Answer 31

prevention surveillance induction of labour before macrosomia attained, in some cases

Question 32

how do you prevent LGA

Answer 32

counsel women about the goals for gestational weight gain women with T1 and T2DM and gestational DM--> tight control of sugars (decreases incidence of LGA) preconceptual counseling for overweight and obese mothers to be counsel obese women to lose weight before pregnancy

Question 33

why is operative vaginal delivery not generally advised in the setting of known macrosomia

Answer 33

incrased risk of shoulder dystocia

Question 34

when is amniotic fluid at maximum volume

Answer 34

800 mL at 28 weeks --> maintained until close to term when it begins to fall to about 500mL at week 50

Question 35

how is the balance of amniotic fluid maintained

Answer 35

production of fetal kidneys and lungs and resorbed by fetal swallowing and interface between membranes and placenta *disturbance in any of these functions may lead to a pathologic change in amniotic fluid volume

Question 36

what is the classic measure of amniotic fluid

Answer 36

amniotic fluid index (AFI) calculated by dividing the maternal abdomen into quadrants and measuring the largest vertical pocket of fluid in each quadrant in cm and summing them AFI of less than 5 is considered oligo--above 20-25 is poly

Question 37

define oligohydramnios

Answer 37

AFI below 5

Question 38

define polyhydramnios

Answer 38

AFI above 20-25

Question 39

why do we care about oligohydramnios

Answer 39

in absence of ROM, it is associated with a 40 fold increase in perinatal mortality partially because without amniotic fluid to cushion it, umbilical cord is more susceptible to compression leading to fetal asphyxiation also associated with congenital abnormalities, especially of GU system, and with growth restriction

Question 40

what are the causes of oligohydramnios

Answer 40

either decreased production or increased withdrawal of amniotic fluid chronic uteroplacental insufficiency (UPI) can lead to oligohydramnios because fetus likely does not have the nutrients or blood volume to maintain an adequate GFR--> UPI commonly assoc with growth restricted infants congenital anomalies of GU tract can lead to decreased urine production --> renal agenesis (potter syndrome), polycystic kidney disease, obstruction most common cause is ROM (should rule this out even if there is no hx of leaking fluid)

Question 41

how do you diagnose oligohydramnios

Answer 41

when AFI less than 5 as measured by U/S

Question 42

how do you manage oligohydramnios

Answer 42

entirely dependent on etiology in pregnancies with IUGR--> need lots of other data (BPP, umbilical artery dopplers, gestational age, cause of IUGR) labour usually induced if at term or post dates if fetus has congenital abnormalities, should refer to maternal-fetal medicine make plan for delivery with pediatrics and pediatric surgeons if there is mec or frequent decels, may do amnioinfusion to increase the AFI

Question 43

why do you do amnioinfusion

Answer 43

if there is mec or frequent decels, may do amnioinfusion to increase the AFI has traditionally been done to dilute any mec present and therefore decrease risk of mec aspiration but this has not been shown to decrease bad outcomes and is decreasingly used for this evidence does suggest that amnioinfusion in the setting of recurrent variable decels does decrease the number of decels caused by cord compression

Question 44

what % of pregnancies have polyhydramnios

Answer 44

2-3%

Question 45

what is polyhydramnios associated with

Answer 45

fetal structural and chromosomal abnormalities maternal diabetes NTDs obstruction of fetal alimentary canal hydrops

Question 46

what causes polyhydramnios

Answer 46

obstruction in fetal GI tract (tracheoesophageal fistula, duodenal atresia) can make fetus unable to swallow fluid increased levels of glucose in diabetic mothers can act as osmotic agent leading to polyhydramnios hydrops secondary to high output cardiac failure is assoc with polyhydramnios monozygotic multiple gestation can lead to twin-to-twin transfusion syndrome with polyhydramnios around one fetus and oligo around the other

Question 47

diagnosis of polyhydramnios

Answer 47

U/S in patient being scanned for size greater than dates, routine screening of diabetic or multiple gestation pregnancies or as an unsuspected finding on a U/S performed for other reasons

Question 48

treatment for polyhydramnios

Answer 48

depends on etiology are at risk for malpresentation should be carefully evaluated during labour increased risk of cord prolapse so ROM should be performed in a controlled setting if possible and only if head is truly engaged in the pelvis make sure to rule out cord prolapse if spontaneous ROM

Question 49

what type of antibodies are Rh antibodies and why does this matter

Answer 49

IgG--> cros the placenta and cause hemolysis of fetal RBCs

Question 50

how does Rh negativity vary among different ethnicities

Answer 50

caucasian--15% african american--8% african--4% native american--1% asia--less than 1% (30% among the basque people of spain)

Question 51

when do most Rh- moms become sensitized (if fetus is Rh+)

Answer 51

only during pregnancy and blood transfusion

Question 52

what is the relationship between ABO incompatibility and Rh sensitization

Answer 52

because there is some transplacental passage of fetal cells in all pregnancies, ABO incompatibility actually decreases the risk of Rh sensitization as a result of the destruction of these fetal cells by Anti-A and anti-B antibodies before mom can mount a response to the Rh antigen

Question 53

why do we care about the hemolytic anemia cause by IgG Rh antobodies

Answer 53

this anemia leads to increased extramedullary production of RBCs ERYTHROBLASTOSIS FETALIS (fetal hydrops) is a syndrome that includes a hyperdynamic state, heart failure and diffuse edema, ascites and pericaridal effusion as the result of serious anemia bilirubin is cleared by the placenta before birth but after birth can cause jaundice and kernicterus after birth

Question 54

what is erythroblastosis fetalis

Answer 54

(fetal hydrops) is a syndrome that includes a hyperdynamic state, heart failure and diffuse edema, ascites and pericaridal effusion as the result of serious anemia

Question 55

define fetal hydrops

Answer 55

accumulation of fluid in the extracellular space in at least two body compartments

Question 56

when should unsensitized Rh- moms be given rhoGAM

Answer 56

any time during the pregnancy is there is a possibility that she may be exposed to fetal blood (amniocentesis, miscarriage, vaginal bleeding, abruption, delivery)

Question 57

what is rhoGAM

Answer 57

anti-D immunoglobulin (Rh IgG)

Question 58

when should rhoGAM be given routinely to an Rh- mom

Answer 58

at 28 weeks and at delivery

Question 59

what is the standard dose of rhoGAM

Answer 59

0.3 mg of Rh IgG eradicates 15mL of fetal RBCs (30 mL of fetal blood with hematocrit of 50)--> adequate for routine pregnancy if there is a placental abruption or antepartum bleeding, a KB test can be sent to actually see how much fetal blood there is and you can respond accordingly with more rhoGAM if needed

Question 60

what do you do if a pregnant Rh- mother has a positive antibody screen

Answer 60

check titers--> Ab titers of aboe 1:16 have been associated with fetal hydrops if paternity is not in question, can do blood type on dad to see what the fetal antigen status is *because about 5% of all pregnancies have unknown or incorrect paternity, safest course is to treat all women as if the fetus is as risk follow titer every 4 weeks during pregnancy--> as long as below 1:16, can manage expectantly if higher than that, serial amniocentesis is begun as early as 16-20 weeks

Question 61

why do we do serial amniocentesis in a sensitized Rh- mom if titer above 1:16

Answer 61

at first amnio, fetal cells can be collected and analyzed for Rh status if negative, fetus can be followed expectantly if Rh+ fetus, fetal anemia is screened for using fetal middle cerebral artery (MCA) doppler measurements (greater blood flow to brain in anemic fetuses)--> if this is high, warrants further investigation due to concern for fetal anemia

Question 62

how do you get a reading for the Liley curve

Answer 62

amniocentesis--> increased bilirubin causes amniotic fluid to absorb more light--> plot results on Liley curve

Question 63

what does zone 1 on Liley curve suggest

Answer 63

mildly affected fetus (due to Rh incompatibility)--> follow up amnio performed every 2-3 weeks

Question 64

what does zone 2 on the Liley curve suggest

Answer 64

moderately affected fetus--> amnio every 1-2 weeks

Question 65

what does zone 3 on Liley curve suggest

Answer 65

severely affected fetus--> once you reach this zone, it is likely the fetus has anemia

Question 66

what is the treatment for fetal anemia

Answer 66

percutaneous umbilical blood sampling (PUBS) and intrauterine transfusion (IUT) PUBS can be used to obtain a fetal hematocrit to verify fetal anemia and to perform an IUT if PUBS or IUT cannot be performed, fetal intraperitoneal transfusion may be performed --> risk of delivery as high at 3% but risk is preferred to the risk of worsening anemia, hydrops and likely fetal death

Question 67

what are some other antigens that can cause problems for the fetus

Answer 67

other RBC antigens (ABO), antigens CDE (D is the Rh antigen), Kell, Duffy and Lewis antigens

Question 68

what antigens cause fetal hydrops

Answer 68

Kell and Duffy *anti Kell antibodies not only lead to a fetal anemia but also to suppression of bone marrow and decreased RBC production

Question 69

what antigens cause mild anemia but not immune hydrops

Answer 69

ABO | Lewis

Question 70

why do we always make sure to deliver IUFD products of conception?

Answer 70

a retained IUFD greater than 3-4 weeks canlead to hypofibrinogenemia secondary to the release of thromboplastic substances from the decomposing fetus in some cases, full blown DIC can occur

Question 71

how do you diagnose IUFD before 20 weeks

Answer 71

"missed abortion" suspected by lack of uterine growth or cessation of symptoms of pregnancy diagnosis confirmed with serially falling beta hCG and U/S documentation

Question 72

how is IUFD diagnosed after 20 weeks

Answer 72

suspected with absence of fetal movements noted by the mother or absence of uterine growth confirmed by U/S *absence of fetal heart motion usually confirmed by 2 clinicians

Question 73

how do you treat IUFD

Answer 73

early gestations evacuated with a D and C or with mifepristone and misoprostol after 20 weeks, usually terminated by induction of labour with prostaglandins or high dose oxytocin

Question 74

what tests can you do to determine cause of fetal death

Answer 74

screening for collagen vascular disorders or hypercoagulable states fetal karyotype TORCH titers autopsy of the fetus *etiology of fetal demise will however usually remain undiagnosed despite testing

Question 75

what is TORCH

Answer 75

``` toxoplasmosis RPR CMV HSV others ```

Question 76

define postterm pregnancy

Answer 76

beyond 42 weeks GA 3-10% of pregnancies will go postterm

Question 77

why do we care about postterm pregnancies

Answer 77

increased risk of macrosomia, meconium aspiration, IUFD, oligohydramnios, dysmaturity syndrome greater risk to mother due to doubled rate of C/S and delivery or large infants

Question 78

most common cause for postterm pregnancy

Answer 78

inaccurate dating but if true postterm--more common in overweight/obese women rare conditions of the fetus associated with postterm--anencephaly, fetal adrenal hypoplasia, absent fetal pituitary --> notable for decreased levels of circulating estrogens

Question 79

can U/S be used to confirm dating at term?

Answer 79

no because can be off by up to 3 weeks accurate dating done by a certain LMP combined with consistency with first or second trimester U/S

Question 80

what is a typical plan for following a postterm pregnancy

Answer 80

1. if past 40 weeks, get NST at 41 weeks --> if nonreassuring, induce labour 2. between 41-42 weeks, get two NSTs or use modified BPP (NST and AFI) --> advantage of this is that oligohydramnios is more likely to be seen prior to a nonreassuring NST and is a marker for poor placental function and may increase the sensitivity of testing for picking up fetuses at risk for IUFD - -induction indicated with nonreassuring fetal testing or can do it electively with an inducible cervix 3. induction of labour at 42 weeks regardless of cervical state

Question 81

what is an inducible cervix

Answer 81

bishop score greater than 6

Question 82

when are most women offered elective induction is postterm

Answer 82

at 41 weeks--leads to lower rates of C/S even if cervix not favorable *remember that active labour may not actually start until 6 cm dilation in an induced patient

Question 83

define monozygotic twins

Answer 83

one fertilized ovum divides into two separate ova

Question 84

define dizygotic twins

Answer 84

ovulation produces two ova and both are fertilized

Question 85

what is the rate of twinning in non assisted pregnancies

Answer 85

1 in 80, with 30% being monozygotic

Question 86

what influences rate of dizygotic twinning

Answer 86

varies between races--> lowest in Asians, intermediate in caucasians and higher in african americans influences by maternal age and parity

Question 87

list some of the complications that can arise with multiple gestation

Answer 87

placenta previa preterm labour cord prolapse PPH cervical incompetence gestational diabetes preeclampsia fetuses are at increased risk of preterm delivery, congenital abnormalities, SGA and malpresentation neonates delivered from multiple gestation weigh less than their singleton peers and have higher overall mortality rate as a result of prematurity and low birth weight

Question 88

what is the average gestational age of delivery for twins

Answer 88

36-37 weeks

Question 89

define monochorionic twins

Answer 89

one placenta

Question 90

define diamniotic twins

Answer 90

two amniotic sacs

Question 91

which type of twins are at most risk of twin transfusion syndrome (TTS)

Answer 91

mono-di twins (monochorionic, diamiotic) --> often have placental vascular communications

Question 92

why do mono-mono twins have an extremely high mortality rate

Answer 92

as high as 40-60% secondary to cord accidents from entanglement (only one placenta and one amniotic sac)

Question 93

when does the division of the fertilized ovum occur to result in di-di monozygotic twins

Answer 93

separation occurs before differentiation of the trophoblast

Question 94

when does the division of the fertilized ovum occur to result in mono-di monozygotic twins

Answer 94

separation occurs after trophoblast differentiation and before amnion formation (days 3-8) results in single placenta, one chorion and two amnions

Question 95

when does the division of the fertilized ovum occur to result in mono-mono monozygotic twins

Answer 95

after amnion formation (days 8-13) this can also rarely lead to conjoined twins if between days 13-15

Question 96

what happens if an ovum splits after day 15 or 16

Answer 96

singleton pregnancy

Question 97

does monozygotic twinning follow an inheritable pattern

Answer 97

no

Question 98

what are the risk factors for monozygotic twinning

Answer 98

slight increase with advancing maternal age and ART (to as high as 5%)

Question 99

what are the risk factors for dizygotic twinning

Answer 99

tend to run in families more common in people of african descent (1 in 1000 in Japan versus 1 in 20 in some nigerian tribes) clomiphene citrate increases rates to up to 8% use of multiple embryos in IVF can lead to increased rates of twinning and higher order multiple gestations in 30-50% of these pregnancies

Question 100

what clinical signs indicate multiple gestation

Answer 100

rapid uterine growth excessive maternal weight gain palpation of three or more large fetal parts on Leopold's b-hCG, human placental lactogen and MSAFP are all elevated for gestational age

Question 101

what forms the twin peak sign on U/S

Answer 101

formed by two placentae fusing together in the setting of di-di twins

Question 102

why are mono-mono twins easy to diagnose

Answer 102

because there are two babies but no intertwin membrane

Question 103

why are multiple gestations managed as high risk pregnancies

Answer 103

high rates of complications *with triplets and higher order pregnancies, selective reduction down to twins or even a singleton pregnancy is often recommended as it reduces the chances of severely premature babies

Question 104

what is poly-oli sequence?

Answer 104

polyhydramnios-oligohydramnios sequence --> aka twin to twin transfusion syndrome results in a small anemic twin and a large, plethoric, polycythemic and occasional hydropic twin etiology is secondary to unequal flow within the vascular communications between twins in their shared placenta--> one twin becomes donor and one is the recipient

Question 105

what are the results of TTTS

Answer 105

one fetus with hypervolemia, cardiomegaly, glomerulotubal hypertrophy, edema and ascites the other fetus with hypovolemia, growth restriction, and oligohydramnios *risk of this syndrome in mono-di twins so serial U/S are done to examine amniotic fluid and fetal growth every 2 weeks after diagnosis

Question 106

how do you manage TTTS

Answer 106

serial amnio reduction, which can reduce preterm contractions secondary to uterine distension and maternal symptoms --> only occasionally cures the fetal symptoms coagulating the communicating fetal vessels has been proposed as treatment in severe cases pregnancy termination is also always offered

Question 107

how are mono-mono twins managed antenatally

Answer 107

risk of cord entaglements and IUFD--> frequent antenatal testing and early delivery even the frequent testing does not seem to make a difference in outcomes though--> thus some women are offered admission to hospital and continuous monitoring from weeks 28-34 when delivery is performed via C/S mono-mono twins and conjoined twins are almost always delivered via C/S

Question 108

what are the 4 possible presentations for twins

Answer 108

both vertex (40%) both breech vertex then breech (40%) breech then vertex when deciding mode of delivery, all breech presenting twins are considered together (20%)

Question 109

how do you deliver twins based on the various possible presentations

Answer 109

1. vertex-vertex--> undergo trial of labour with C/S reserved for unusual indications; placental abruption can sometimes occur with the second vertex twin 2. vertex-breech--> can undergo trial of labour is twins are concordant or if presenting twin is larger; twins should be between 1500-3500 g - -> breech presentation for twin B has advantages for delivery of second twin as their lower extremity can be grabbed and pulled out