Fetal Complications of Pregnancy Flashcards
how do you estimate antepartum fetal weight
U/S
define small for gestational age (SGA)
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
define large for gestational age (LGA)
fetuses whose estimated birth weight is above the 90th percentile
what are the two types of SGA
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)
by term, what volume of maternal cardiac output is passing through the placental exchange network per minute
600 mL/min
what determines the ultimate growth potential of the fetus
genetics
when the expected regulatory processes occur in the fetus, mother and placenta, normal growth ensues
why do we care about SGA
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
what are the two causative categories of SGA
- decreased growth potential
2. IUGR
risk factors for decreased growth potential causing SGA
genetic and chromosomal abnormalities
intrauterine infection
teratogenic exposure
substance use
radiation exposure
small maternal stature
pregnancy at high altitudes
female fetus
risk factors for IUGR causing SGA
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
what % of decreased growth potential SGA is caused by congenital abnormalities (i.e the trisomies)
10-15%
i.e Down, Patau, Edward, Turner, osteogenesis imperfecta, achondroplasia, NTDs, anancephaly and other autosomal recessive disorders
name some intrauterine infections that can leads to decreased growth potential SGA
CMV
rubella
probably account for 10-15% of all SGA babies
what are the two most common teratogens that cause decreased growth potential SGA
alcohol and cigarettes
what % of babies diagnosed with decreased growth potential SGA are just constitutionally small
10%
based on parental stature or genetic potential
appears to vary by race/ethnicity
what two general types of growth occur in utero, and when do they happen
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
what do we think causes asymmetric growth
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
when should you get an U/S to investigate fetal growth
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
how do you manage a fetus suspected of being SGA/IUGR, and how can you use U/S to distinguish the two
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
what might cause absent or reversed diastolic flow in the umbilical artery on doppler
calcified or thrombosed placenta
how are patients at risk for SGA due to placental insufficiency, preeclampsia, collagen vascular disorders or vascular disease often treated
with low dose aspirin
how are patients at risk for SGA due to history of prior placental thrombosis, thrombophilias, or antiphospholipid antibody syndrome treated
heparin and corticosteroids as well as low dose aspirin
mixed results
is there a reason to expedite delivery of fetuses who have been small throughout gestation
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)
which is more important–dx of fetal macrosomia or LGA
fetal macrosomia–> greater risk for birth trauma or C/S
what is the definition of fetal macrosomia
vary–> ACOG uses BIRTH WEIGHT ABOVE 4500 g
others use birth weights above 4000 g or 4200 g
what are the risks associated with fetal macrosomia
shoulder dystocia
birth trauma with resultant brachial plexus injuries with vaginal deliveries
low apgar scores
hypoglycemia
polycytheia
hypocalcemia
jaundice
what are the risks associated with LGA babies in infancy
childhood leukemia
wilms tumour
osteosarcoma
what are the risks to mom with LGA/macrosomic fetuses
C/S risk higher (failure to progress)
perineal trauma
post partum hemorrhage
what is the most classic risk factor for fetal macrosomia
preexisting or gestational diabetes mellitus
list the risk factors for fetal macrosomia
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)
is U/S a good tool for screening for LGA infants
not really–PPV is only 50% for LGA infants (more useful for SGA fetuses)
how do you manage LGA/macrosomia
prevention
surveillance
induction of labour before macrosomia attained, in some cases
how do you prevent LGA
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
why is operative vaginal delivery not generally advised in the setting of known macrosomia
incrased risk of shoulder dystocia
when is amniotic fluid at maximum volume
800 mL at 28 weeks –> maintained until close to term when it begins to fall to about 500mL at week 50
how is the balance of amniotic fluid maintained
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
what is the classic measure of amniotic fluid
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
define oligohydramnios
AFI below 5
define polyhydramnios
AFI above 20-25
why do we care about oligohydramnios
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
what are the causes of oligohydramnios
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)
how do you diagnose oligohydramnios
when AFI less than 5 as measured by U/S
how do you manage oligohydramnios
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
why do you do amnioinfusion
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
what % of pregnancies have polyhydramnios
2-3%
what is polyhydramnios associated with
fetal structural and chromosomal abnormalities
maternal diabetes
NTDs
obstruction of fetal alimentary canal
hydrops
what causes polyhydramnios
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
diagnosis of polyhydramnios
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
treatment for polyhydramnios
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
what type of antibodies are Rh antibodies and why does this matter
IgG–> cros the placenta and cause hemolysis of fetal RBCs
how does Rh negativity vary among different ethnicities
caucasian–15%
african american–8%
african–4%
native american–1%
asia–less than 1%
(30% among the basque people of spain)
when do most Rh- moms become sensitized (if fetus is Rh+)
only during pregnancy and blood transfusion
what is the relationship between ABO incompatibility and Rh sensitization
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
why do we care about the hemolytic anemia cause by IgG Rh antobodies
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
what is 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
define fetal hydrops
accumulation of fluid in the extracellular space in at least two body compartments
when should unsensitized Rh- moms be given rhoGAM
any time during the pregnancy is there is a possibility that she may be exposed to fetal blood (amniocentesis, miscarriage, vaginal bleeding, abruption, delivery)
what is rhoGAM
anti-D immunoglobulin (Rh IgG)
when should rhoGAM be given routinely to an Rh- mom
at 28 weeks and at delivery
what is the standard dose of rhoGAM
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
what do you do if a pregnant Rh- mother has a positive antibody screen
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
why do we do serial amniocentesis in a sensitized Rh- mom if titer above 1:16
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
how do you get a reading for the Liley curve
amniocentesis–> increased bilirubin causes amniotic fluid to absorb more light–> plot results on Liley curve
what does zone 1 on Liley curve suggest
mildly affected fetus (due to Rh incompatibility)–> follow up amnio performed every 2-3 weeks
what does zone 2 on the Liley curve suggest
moderately affected fetus–> amnio every 1-2 weeks
what does zone 3 on Liley curve suggest
severely affected fetus–> once you reach this zone, it is likely the fetus has anemia
what is the treatment for fetal anemia
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
what are some other antigens that can cause problems for the fetus
other RBC antigens (ABO), antigens CDE (D is the Rh antigen), Kell, Duffy and Lewis antigens
what antigens cause fetal hydrops
Kell and Duffy
*anti Kell antibodies not only lead to a fetal anemia but also to suppression of bone marrow and decreased RBC production
what antigens cause mild anemia but not immune hydrops
ABO
Lewis
why do we always make sure to deliver IUFD products of conception?
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
how do you diagnose IUFD before 20 weeks
“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
how is IUFD diagnosed after 20 weeks
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
how do you treat IUFD
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
what tests can you do to determine cause of fetal death
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
what is TORCH
toxoplasmosis RPR CMV HSV others
define postterm pregnancy
beyond 42 weeks GA
3-10% of pregnancies will go postterm
why do we care about postterm pregnancies
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
most common cause for postterm pregnancy
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
can U/S be used to confirm dating at term?
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
what is a typical plan for following a postterm pregnancy
- if past 40 weeks, get NST at 41 weeks –> if nonreassuring, induce labour
- 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 - induction of labour at 42 weeks regardless of cervical state
what is an inducible cervix
bishop score greater than 6
when are most women offered elective induction is postterm
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
define monozygotic twins
one fertilized ovum divides into two separate ova
define dizygotic twins
ovulation produces two ova and both are fertilized
what is the rate of twinning in non assisted pregnancies
1 in 80, with 30% being monozygotic
what influences rate of dizygotic twinning
varies between races–> lowest in Asians, intermediate in caucasians and higher in african americans
influences by maternal age and parity
list some of the complications that can arise with multiple gestation
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
what is the average gestational age of delivery for twins
36-37 weeks
define monochorionic twins
one placenta
define diamniotic twins
two amniotic sacs
which type of twins are at most risk of twin transfusion syndrome (TTS)
mono-di twins (monochorionic, diamiotic) –> often have placental vascular communications
why do mono-mono twins have an extremely high mortality rate
as high as 40-60%
secondary to cord accidents from entanglement (only one placenta and one amniotic sac)
when does the division of the fertilized ovum occur to result in di-di monozygotic twins
separation occurs before differentiation of the trophoblast
when does the division of the fertilized ovum occur to result in mono-di monozygotic twins
separation occurs after trophoblast differentiation and before amnion formation (days 3-8)
results in single placenta, one chorion and two amnions
when does the division of the fertilized ovum occur to result in mono-mono monozygotic twins
after amnion formation (days 8-13)
this can also rarely lead to conjoined twins if between days 13-15
what happens if an ovum splits after day 15 or 16
singleton pregnancy
does monozygotic twinning follow an inheritable pattern
no
what are the risk factors for monozygotic twinning
slight increase with advancing maternal age and ART (to as high as 5%)
what are the risk factors for dizygotic twinning
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
what clinical signs indicate multiple gestation
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
what forms the twin peak sign on U/S
formed by two placentae fusing together in the setting of di-di twins
why are mono-mono twins easy to diagnose
because there are two babies but no intertwin membrane
why are multiple gestations managed as high risk pregnancies
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
what is poly-oli sequence?
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
what are the results of TTTS
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
how do you manage TTTS
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
how are mono-mono twins managed antenatally
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
what are the 4 possible presentations for twins
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%)
how do you deliver twins based on the various possible presentations
- vertex-vertex–> undergo trial of labour with C/S reserved for unusual indications; placental abruption can sometimes occur with the second vertex twin
- 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
