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Obstetrics and Gynecology > Fetal Complications of Pregnancy > Flashcards

Fetal Complications of Pregnancy Flashcards

1
Q

how do you estimate antepartum fetal weight

A

U/S

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2
Q

define small for gestational age (SGA)

A

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

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3
Q

define large for gestational age (LGA)

A

fetuses whose estimated birth weight is above the 90th percentile

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4
Q

what are the two types of SGA

A

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)

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5
Q

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

A

600 mL/min

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6
Q

what determines the ultimate growth potential of the fetus

A

genetics

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

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7
Q

why do we care about SGA

A

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

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8
Q

what are the two causative categories of SGA

A
  1. decreased growth potential

2. IUGR

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9
Q

risk factors for decreased growth potential causing SGA

A

genetic and chromosomal abnormalities

intrauterine infection

teratogenic exposure

substance use

radiation exposure

small maternal stature

pregnancy at high altitudes

female fetus

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10
Q

risk factors for IUGR causing SGA

A 
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
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11
Q

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

A

10-15%

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

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12
Q

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

A

CMV

rubella

probably account for 10-15% of all SGA babies

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13
Q

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

A

alcohol and cigarettes

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14
Q

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

A

10%

based on parental stature or genetic potential

appears to vary by race/ethnicity

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15
Q

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

A

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

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16
Q

what do we think causes asymmetric growth

A

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

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17
Q

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

A

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

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18
Q

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

A

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

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19
Q

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

A

calcified or thrombosed placenta

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20
Q

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

A

with low dose aspirin

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21
Q

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

A

heparin and corticosteroids as well as low dose aspirin

mixed results

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22
Q

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

A

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)

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23
Q

which is more important–dx of fetal macrosomia or LGA

A

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

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24
Q

what is the definition of fetal macrosomia

A

vary–> ACOG uses BIRTH WEIGHT ABOVE 4500 g

others use birth weights above 4000 g or 4200 g

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25
Q

what are the risks associated with fetal macrosomia

A

shoulder dystocia

birth trauma with resultant brachial plexus injuries with vaginal deliveries

low apgar scores

hypoglycemia

polycytheia

hypocalcemia

jaundice

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26
Q

what are the risks associated with LGA babies in infancy

A

childhood leukemia

wilms tumour

osteosarcoma

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27
Q

what are the risks to mom with LGA/macrosomic fetuses

A

C/S risk higher (failure to progress)

perineal trauma

post partum hemorrhage

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28
Q

what is the most classic risk factor for fetal macrosomia

A

preexisting or gestational diabetes mellitus

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29
Q

list the risk factors for fetal macrosomia

A

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)

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30
Q

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

A

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

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31
Q

how do you manage LGA/macrosomia

A

prevention

surveillance

induction of labour before macrosomia attained, in some cases

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32
Q

how do you prevent LGA

A

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

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33
Q

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

A

incrased risk of shoulder dystocia

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34
Q

when is amniotic fluid at maximum volume

A

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

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35
Q

how is the balance of amniotic fluid maintained

A

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

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36
Q

what is the classic measure of amniotic fluid

A

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

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37
Q

define oligohydramnios

A

AFI below 5

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38
Q

define polyhydramnios

A

AFI above 20-25

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39
Q

why do we care about oligohydramnios

A

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

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40
Q

what are the causes of oligohydramnios

A

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)

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41
Q

how do you diagnose oligohydramnios

A

when AFI less than 5 as measured by U/S

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42
Q

how do you manage oligohydramnios

A

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

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43
Q

why do you do amnioinfusion

A

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

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44
Q

what % of pregnancies have polyhydramnios

A

2-3%

45
Q

what is polyhydramnios associated with

A

fetal structural and chromosomal abnormalities

maternal diabetes

NTDs

obstruction of fetal alimentary canal

hydrops

46
Q

what causes polyhydramnios

A

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

47
Q

diagnosis of polyhydramnios

A

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

48
Q

treatment for polyhydramnios

A

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

49
Q

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

A

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

50
Q

how does Rh negativity vary among different ethnicities

A

caucasian–15%

african american–8%

african–4%

native american–1%

asia–less than 1%

(30% among the basque people of spain)

51
Q

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

A

only during pregnancy and blood transfusion

52
Q

what is the relationship between ABO incompatibility and Rh sensitization

A

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

53
Q

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

A

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

54
Q

what is erythroblastosis fetalis

A

(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

55
Q

define fetal hydrops

A

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

56
Q

when should unsensitized Rh- moms be given rhoGAM

A

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

57
Q

what is rhoGAM

A

anti-D immunoglobulin (Rh IgG)

58
Q

when should rhoGAM be given routinely to an Rh- mom

A

at 28 weeks and at delivery

59
Q

what is the standard dose of rhoGAM

A

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

60
Q

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

A

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

61
Q

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

A

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

62
Q

how do you get a reading for the Liley curve

A

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

63
Q

what does zone 1 on Liley curve suggest

A

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

64
Q

what does zone 2 on the Liley curve suggest

A

moderately affected fetus–> amnio every 1-2 weeks

65
Q

what does zone 3 on Liley curve suggest

A

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

66
Q

what is the treatment for fetal anemia

A

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

67
Q

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

A

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

68
Q

what antigens cause fetal hydrops

A

Kell and Duffy

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

69
Q

what antigens cause mild anemia but not immune hydrops

A

ABO

Lewis

70
Q

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

A

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

71
Q

how do you diagnose IUFD before 20 weeks

A

“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

72
Q

how is IUFD diagnosed after 20 weeks

A

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

73
Q

how do you treat IUFD

A

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

74
Q

what tests can you do to determine cause of fetal death

A

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

75
Q

what is TORCH

A 
toxoplasmosis
RPR
CMV
HSV
others
76
Q

define postterm pregnancy

A

beyond 42 weeks GA

3-10% of pregnancies will go postterm

77
Q

why do we care about postterm pregnancies

A

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

78
Q

most common cause for postterm pregnancy

A

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

79
Q

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

A

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

80
Q

what is a typical plan for following a postterm pregnancy

A
  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
81
Q

what is an inducible cervix

A

bishop score greater than 6

82
Q

when are most women offered elective induction is postterm

A

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

83
Q

define monozygotic twins

A

one fertilized ovum divides into two separate ova

84
Q

define dizygotic twins

A

ovulation produces two ova and both are fertilized

85
Q

what is the rate of twinning in non assisted pregnancies

A

1 in 80, with 30% being monozygotic

86
Q

what influences rate of dizygotic twinning

A

varies between races–> lowest in Asians, intermediate in caucasians and higher in african americans

influences by maternal age and parity

87
Q

list some of the complications that can arise with multiple gestation

A

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

88
Q

what is the average gestational age of delivery for twins

A

36-37 weeks

89
Q

define monochorionic twins

A

one placenta

90
Q

define diamniotic twins

A

two amniotic sacs

91
Q

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

A

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

92
Q

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

A

as high as 40-60%

secondary to cord accidents from entanglement (only one placenta and one amniotic sac)

93
Q

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

A

separation occurs before differentiation of the trophoblast

94
Q

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

A

separation occurs after trophoblast differentiation and before amnion formation (days 3-8)

results in single placenta, one chorion and two amnions

95
Q

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

A

after amnion formation (days 8-13)

this can also rarely lead to conjoined twins if between days 13-15

96
Q

what happens if an ovum splits after day 15 or 16

A

singleton pregnancy

97
Q

does monozygotic twinning follow an inheritable pattern

A

no

98
Q

what are the risk factors for monozygotic twinning

A

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

99
Q

what are the risk factors for dizygotic twinning

A

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

100
Q

what clinical signs indicate multiple gestation

A

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

101
Q

what forms the twin peak sign on U/S

A

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

102
Q

why are mono-mono twins easy to diagnose

A

because there are two babies but no intertwin membrane

103
Q

why are multiple gestations managed as high risk pregnancies

A

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

104
Q

what is poly-oli sequence?

A

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

105
Q

what are the results of TTTS

A

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

106
Q

how do you manage TTTS

A

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

107
Q

how are mono-mono twins managed antenatally

A

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

108
Q

what are the 4 possible presentations for twins

A

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%)

109
Q

how do you deliver twins based on the various possible presentations

A
  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

Obstetrics and Gynecology (21 decks)

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