OB Flashcards
where is AFP produced
fetal yolk sac and liver
what is elevated AFP
> 2.5 MoM (multiples of median)
What causes increase in AFP?
What about decrease
Increase: open NTD, abd wall defect, multiples, fetal maternal hemorrhage, germ cell tumor, fetal demise, placental conditions, underestimation of GA
Decrease with T21
what should you do if you have elevated MSAFP
evaluate with US, correct GA consider amnio
Dont need increased antenatal surveillance based on isolated elevated AFP
Criteria for breech vaginal delivery
counseled on risk of cord prolapse or head entrapment
37weeks plus
No prior CD
2500-4000g
frank or complete breech
normal AFI
adequate pelvis
no fetal anomalies
non hyperextended neck
spontaneous/normal labor course
experienced provider
% of preg breech
% of CS for breech
3-4 % of pregnancies are breech
17% of CS due to breech
risk of fetal death with FGR <10% and <5%ile
<10: 1.5%
<5: 2.5%
risk of recurrence for prior preg with FGR
20%
when to offer genetic counseling +/- amnio for FGR
-diagnosed before 32w
-FGR + poly
-fetal malformation
Major markers for T21
duodenal atresia
Cardiac (ASD, TOF, AV canal defects)
Soft markers
Which have the highest liklihood ratios
Which one is the best predictor
echogenic cardiac focus
pyelectasis
short femur length
choroid plexus cyst
echogenic bowel, thickened NT, and ventriculomegaly even when isolated are higher likelihood ratio
isolated finding of thickened nuchal skin highest risk of aneuploidy
what is the importance of NT and nasal bone
NT detection rate for T21 being 64-70%
cystic hygroma associated with T21 in about 50% of cases
Hypoplastic or absent nasal bone can be detected in 62-70% of fetuses with down syndrome, only 1% of normal fetuses
1/3 of cases with thickened NT will have chromosomal defects, T21 accounts for 50% of those
omphalacele
1:5000
midline defect in abdominal contents herniate
covered by amnion and peritoneum
has liver herniation
can look like normal embryo at 9-11 weeks
50% associated with cardiac defects
defects larger than 5 cm delivered by CS
umbilical cord insertion at apex of defect
gastroschisis
1:2500
full thickness defect, R paraumbilical
no liver herniation
no overlying membrane
never looks like normal embryo
no increase in chromosomal abnormalities
can deliver vaginally, immediate repair. can be done if you can return abd contents, in about 80% of cases
when to change EDD based on GA and CRL discrepancy from LMP
if < 9w, change if more than 5d
from 9-15w6d, change if more than 7d
from 16w-21w6d, change if more than 10d
from 22w to 27w6d change if more than 14d
from 28w and up, change if more than 21d
risk factors for NTDs
-environmental factors
-medications (anti epileptics carbamazepine, valproic acid)
-maternal hyperthermia
-obesity
-hispanic population
-genetics. chances if 1 prior sibling is 3.2%, two prior is 10%
what women are at high risk of NTD and what dose should they take
4 mg (4000 mcg) 3 mo before pregnancy and continue until 12w
women with previous preg affected by NTD
women who are affected by NTD themselves
those who have a partner affected
those who have a partner with a previous affected child
folate resistant NTDs
poor glucose control in first trimester
hyperthermia
obesity
aneuploidy
genetic disorders
those on anti epileptic meds
Delivery timing for FGR
EFW 3-10%, no concurrent findings
38-39 w0d per smfm (39w6d per acog)
delivery timing for EFW <3%ile, no concurrent findings
37w or at time of diagnosis if later
Elevated UAD delivery timing
37 weeks
Absent end diastolic flow delivery timing
33-34w
reversed end diastolic flow delivery timing
30-32w
delivery timing with FGR and concurrent conditions (oligo, preeclampsia, cHTN)
34-37w6d
What are the causes of FGR
Maternal- cHTN, pregestational DM, Renault insufficiency, AI dz, PIH, substance abuse, teratogens
Placental- abruption, SUA, velamentous or marginal cord, TTS
Fetal- multiples, chromosome abnormalities, structural anomalies (cardiac, anencephaly), infections
delivery timing for uncomplicated di/di twins
38-38w6d
delivery timing for di/di twins, complicated
individualized
delivery timing for mo/di uncomplicated
34-37w6d
delivery timing for mo/di complicated
32-34w0d by CD
Clinical presentation of toxo ?
Diagnosis?
intracranial calcification
chorioretinitis
hepatosplenomegaly
hearing loss
low IQ/neurodevelopmental issues
(All head problems)
Igm- only that pos is acute infection
If iGG pos and igm neg- immunity from previous infection
CMV clinical presentation
chorioretinitis
hepatosplenomegaly
abdominal and liver calcifications
FGR
fetal hydrops
echogenic bowel
ventriculomegaly
Parvovirus
what is the pathophysiology
Vertical transmission rate
Presentation
Diagnosis
Treatment
fetal survival rate
virus replicated in bone marrow, causes anemia, heart failure and hydrops
50% of population is immune (IgG positive)
vertical transmission is 25%
infection in first ti > spontaneous abortion
in late 2nd and 3rd tri > hydrops and IUFD
Mom: rash, arthritis, flu like illness, most asx
diagnosis: ELISA for IgG and IgM. PCR of amniotic fluid is more sensitive.
Igg pos- immune
If both igg and igm both positive or both neg- monitor for signs of infection. Repeat testing in 4 weeks.
Tx: PUBS looking for anemia and psb transfusion if hydrops
serial weekly US for fetal well being, rule out hydrops for 2 months after exposure. MCA doppler studies to assess degree of anemia
Fetal survival w/ treatment: 80%, w/o treatment 20-50%
treatment for toxo
spiramycin to decrease placental transfer
treat affected infant with pyrimethamine, sulfadiazine, folinic acid for one year
varicella pneumonia
20% of pregnant women with varicella, mortality 5-15%
treat with IV acyclovir and ICU admission
postexposure ppx for varicella non immune pregnant patients
VZIG within 10 days, ideally within 96h OR acyclovir (800 mg PO 5x daily for 7d)
Diagnosis of cmv
transmission rate for primary CMV
Recurrent CMV?
Igm is not reliable
Get igG and avidity testing
High avidity- infection more than 6 months ago. Low avidity- infection less than 2-4 months ago.
If you have a pos IgM- can be new or chronic cmv
Primary: 30%. 30% of infected fetuses, neonatal dz will occur. Of all infected neonates, 305% will die
Secondary: <2%, negligible
when is the highest risk for neonatal effects with maternal varicella infection
if maternal infection is <5 days before delivery (no time for passive immunity) or 2 days after
high rate of neonatal infection if preg woman infected and delivery before or after onset of rash
Give VZIG to neonate delivered by mom with varicella 5 days before to 2 days after delivery.
IV acyclovir to baby if signs of neonatal infection
quad screen results for second trimester screen
T21
T18
T21: high HCG, estriol low, inhibin up, MSAFP down
T18: HCG down, estriol down, inhibin NA, MSAFP down
what is first trimester screening
NT
HCG
PAPP-A
integrated screening
PAPP-A with NT AND second trimester screen
-results collected but not reported until all tests done. sensitivity 95%
-without NT, serum integrated screen, sensitivity 85-88%
what is sequential screening
first trimester screen pos: offer diagnostic testing
first tri screen neg: second tri screening offered
sensitivity 95%
Final risk assessment incorporates both tests
CVS vs amnio
amnio: can screen for AFP and diagnosis NTD, CVS cannot
amnio tests individual cells, CVS does tissue
amnio: after 15w, CVS at 10-12w
karyotype vs FISH vs Chromosome microarray
karyotype: chromosome abnormalities, culture cells
FISH: CH 13, 18, 21, X, Y. Confirmatory cultures cells
Miroarray: copy number variants (duplicated or deleted sections of DNA). living cells not required, preferred test for stillbirth
situations that require VTE ppx in preg and pp
-hx of unprovoked VTE
-low risk thromophilia with single previous episode of VTE
-high risk thromophilia w/o prior VTE (FVL homozygous, prothrombin homozygous, heterzygous for FVL and prothrombin, antithrombin deficiency)
-high risk thrombophilia with prior VTE
-two or more episodes of VTE (get intermediate or therapeutic dosing)
-two or more episodes of VTE (receiving long term anticoag, get adjusted dose )