Ch 7 Fetal complications of pregnancy Flashcards
fetus < 10th percentile are sga
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fetuses whose efw > 90th% are lga
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sga fetuses are described as either symmetric or asymmetric.
symmetric means fetus is proportionally small
asymmetric imples certain organs of fetus are disproportionately small
asymmetric infant will have wasting of torso and extremities while preserving the brain.
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sga infants do better than infants with the same weight delivered at earlier gestational ages.
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congential abnormalities account for approximately 10-15% of SGA infants. Trisomy 21 ( down syndrome), trisomy 18, and trisomy 13 all lead to SGA babies. Turner syndrome, 45xo, leads to a decrease in birth weight.
many intrauterine infections - cytomegalovirus and rubella lead to SGA.
exposure to tertogens, most chemotherapeutic agents, and other drugs during pregnancy can also lead to decreased growth potential .
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asymmetric growth is presumably caused by decreased nutrition and oxygen being transmitted across the placenta, when is then shunted to the fetal brain. 2/3 of the tim growth restriction is asymmetric and can be identified by increased head-to-abdominal measurement
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maternal risk factors for sga:
HTN, anemia, chronic renal disease, antiphospholipid antibody syndrome, systemic lupus erythematosus, and severe malnutrition
severe diabetes with extensive vascular disease may also lead to IUGR.
placental factors leading to diminished placental blood flow may lead to IUGR
placenta previa, velamentous and marginal cord insertion, placental thrombosis with or without infaction.
multiple gestations lead to lower birth weights because of earlier delivery and SGA infants.
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a fetus with decreased growth potential will start small and stay small, wherease one with IUGR will progressively fall off the growth curve. another test to differentiate IUGR fetuses is
Doppler investigation of umbilical artery.
normal flow through umbilical artery is higher during systole and decreases only 50% to 80% during diastole. flow during diastole should never be absent or reversed.
in setting of increased placental resistance, which can be seen with thrombosed or calcified placenta, diastolic flow decreases or even becomes absent or reversed. reversed diastolic flow is particularly concerning and is associated with high risk of intrauterine fetal demise
SGA fetus with normal doppler value is often expectantly managed to term, whereas those with abnormal dopper values are often delivered early.
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treatment for patients with hx of SGA:
underlying etiology should be explored
if malnutrition or drugs like alcohol / cigarettes these should be dealt with at each prenatal visitl.
pt with hx of placenta insufficiency, preeclampsia, collagen vacscular disorders, or vascular disease are often treated with low dose aspirin.
pt with prior placental thrombosis, thrombopilias, or antiphospholipid antibody syndrome have been treated with heparin and corticosteroids as well, with mixed results
polyhydramnios, afi > 20-25, present in 2-3 % of pregnancies. fetal structural and chromosomal abnormalities are more common in polyhydramnios. it is associated with maternal diabetes and malformations such as neural tube defects, obstruction of fetal alimentary canal, fetal hydrops; however, majority of cases of polyhydramnios have no associated diagnosis or cause
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polyhydramnios is not as ominous a sign as oligohydramnios
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polyhydramnios is associated with increase in congenital anomalies
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associated with diabetes, hydrops, multiple gestation. an obstruction of gastrointestinal tract (e.g. tracheoesophageal fistula, duodenal atresia) may render fetus unable to swallow the amniotic fluid.
increased levels of circulating glucose can act as osmotic diuretic in the fetus, leading to polyhydramnios.
monozygotic multiple gestation can lead to twin-to-twin transfusion syndrome with polyhydramnios around one fetus and oligohydramnios around the other.
polyhydramnios has been associated with stillbirth and preeclampsia
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polyhydramniso are at risk for malprsentation and should be carefully evaluated during labor. there is an increased risk of cord prolapse with polyhydramnis. rom should be performed in controlled setting if possible and only if head is truly engaged in pelvis.
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if woman RH negative, fetus is RH positive either in previous or current pregnancy, shemay become sensitized to RH antigen
may also become sensitized from blood transfusion and develop anti RH antibodies.
these IgG antibodies cross the placenta and cause HEMOLYSIS OF FETAL RBC WHO IS RH POSITIVE.
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if patient is RH negative but has NEGATIVE antibody screen, the goal during pregnancfy is to keep her from becoming sensitized. any tim during the pregnancy, if there is apossibility that a patient may be exposed to fetal blood, such as amniocentesis, miscarriage, vaginal bleeding, abruption and delivery she should be given rhoGAM, an antiD immunoglobulin (rh IgG). rhogam should be administered at 28 weeks and postpartum if the neonate is Rh positive.
rhogam 0.3mg of Rh IgG will eradicate 15ml of fetal RBC. (adequate for routine pregnancy)
however, in the setting of placental abruption or any antepartum bleeding, a kleihauer-betke test for the amount of fetal RBCs in maternal circulation can be sent. if amt of fetal rbcs more than what we eliminated by single rhogam, additional dosages can be given
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there are a variety of other rbc antigens including
ABO blood type
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sensitized patients are managed similar to rh-negative patients with:
antibody titers
MCA doppler measuremetns
pubs
transfusions
when there is no explanation for a fetal demise, it is usually attributed to a “cord accident”
a retained iufd > 3-4 weeks can lead to hypofibrinogenemia secondary to release of thromboplastic substances from decomposing fetus. full-blown disseminated intravascular coagulation (DIC) can result
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