Fetal complications of pregnancy Flashcards
Growth disorders
If fundal ht differs by 3cm or more, get an U/S
SGA
< 10th %ile
Symmetric = think early insult
Asymmetric = think later
Skull > rest of body
Decreased growth potential
Trisomies, Turner, OI (osteogenesis imperfect), achondroplasia, NTDs, anencephaly, or intrauterine infections like CMV / rubella, or teratogens like chemo
IUGR:
Generally asymmetric (not enough nutrients getting across)
A/w smoking, antiphospholipid Ab, SLE, malnutrition, severe chronic renal dz, HTN, anemia in mom, or placental insufficiency (previa / marginal insertion / thrombosis +/- infarction), or multiples
Check cord doppler to see how placenta’s doing
Twin-twin transfusion should be suspected if
One big, one small twin
Monitor SGA with fetal testing
NST/OCT (oxytocin challenge test), BPP, and/or umbilical doppler
LGA
> 90th %ile
Macrosomia
= birth wt > 4,500g officially, but some use other definitions - e.g. to offer C/S if 3500g in diabetic mom, or 4000g otherwise
Risks of macrosomia
Big risk shoulder dystocia, brachial plexus injuries, low Apgars, hypoglycemia, polycythemia, hypoCa, jaundice; also childhood leukemia, Wilms tumor, osteosarcoma
Macrosomia is associated with
Maternal obesity, gDM or cDM, postterm, multiparity, AMA
Amniotic fluid disorders:
Max volume 800mL @ 28wks, then falls to 400mL by 40wks
AFI normal range: 5 to 20-25 (varies by EGA)
Oligohydramnios: Definition
AFI < 5
Oligohydramnios: Presenting symptoms
See nonreactive NST, FHR decels, meconium
Can lead to cord compression!
Oligohydramnios: Etiology
Not making (GU disorders: renal agenesis, polycystic kidney, obstruction; also chronic uteroplacental insufficiency) or losing too much (ROM) amniotic fluid.
Oligohydramnios: Management
Check BPP, cord doppler, U/S for anomalies
Induce if ROM at term
Can do amnioinfusion to decrease # of variable decels / “dilute meconium”
● Polyhydramnios: Definition
AFI > 20-25
Not as worrisome.
Polyhydramnios: Etiology
Not swallowing (GI tract abnormality, duodenal atresia), or making too much (infants of diabetic mothers → osmotic diuretic; or high-output cardiac failure / TTTS- twin twin transfusion syndrome)
Polyhydramnois: risk
Risk of cord prolapse
Only AROM if sure that head is engaged; check for cord after SROM
Rh incompatibility Management
All this applies to Rh negative moms only
RhoGAM (anti-D IgG)
If already sensitized, follow with middle cerebral artery dopplers (faster = more anemic); (spectrophotometer is another way, older)
Can do PUBS (Percutaneous Umbilical Cord Blood Sampling) / in utero transfusion if really anemic
When to give RhoGAM
At 28 wks
Postpartum if neonate is Rh positive
Any time there’s bleeding!
What is the dose of RhoGAM?
0.3mg = 1 dose
How much fetal RBCs dose one dose of RhoGAM eradicate?
1 dose = eradicates 15 mL fetal RBCs. Good enough for normal delivery
Can do Kleihauer-Betke to quantify if abruption, antepartum bleeding
Hydrops
Erythroblastosis fetalis
Heart failure, diffuse edema, fluid in 2+ compartments (ascites /pleural / pericardial effusions), all 2/2 anemia. Jaundice / neurotoxic effects of bilirubin too, but only after delivery (placenta clears it during pregnancy)
Other causes of hydrops
Manage all with antibody titers, amnio, MCA doppler, PUBS / transfusion
Kelly kills = anti-Kell1 = hydrops
Duffy dies = anti-Duffy = hydrops
Lewis lives = anti-Lewis = cause mild hemolytic anemia
ABO causes mild hemolysis too
Fetal demise Dx
If no explanation, usually attributed to a “cord accident”
Dx: lack of uterine growth, falling hCG, U/S (<20wks) or lack of fetal movement (> 20 wks)
Fetal demise risk after 3-4 weeks
If > 3-4 wks, can lead to hypofibrinogenemia 2/2 release of thromboplastic substance from decomposing fetus, and even to DIC! so get a fibrinogen level!
Fetal demise & multiples:
If one baby dies in utero, check fibrinogen level qweek / biweekly, esp if unusual bleeding (fibrinogen may decrease → coagulopathy!)
Spalding sign
Overlapping of fetal skull bones suggesting fetal demise
Tx of fetal demise
D&E if early, or induction of labor (prostaglandins / high dose oxytocin) if late.
Work up after fetal demise
Test for TORCH, fetal karyotype, screen for collagen vascular dz / coagulopathies, get fetal autopsy
Postterm pregnancy:
> 42 wks. Get a nst at 40 and 41 weeks - don’t just send home!
Risks of postterm pregnancy
Higher risk to mom & baby
Macrosomia, oligo, meconium aspiration, intrauterine demise, dysmaturity syndrome - look like old man!
1 cause of postterm pregnancy
Inaccurate dating
Management of postterm pregnancy
Manage with more frequent visits, fetal testing (NST in wk 40, BPP & NST in 2 visits in wk 41)
Induce if nonreassuring testing or electively if Bishop > 6 @ wks 40-41; or no matter what > 42
Risk of multiples:
Higher risk preterm delivery, congenital abnormalities, SGA, malpresentation.
Twins delivery
Usually wks 36-37
Push up testing too
Twin delivery: Can do TOL if vtx/vtx or vtx/breech if twins concordant / presenting twin is larger & vtx (grab smaller second twin & pull out breech!)
Triplets delivery
Usually wks 33-34
Push up testing too!
Triplet delivery: only if vtx/vtx/vtx (rare), usually C/S. Also C/S for more than 3.
Dizygotic twins:
2 ova, 2 sperm. increased FSH can be hereditary, so dizygotic twins can be too
Monozygotic twins:
Division of fertilized egg
Dichorionic / diamniotic
DiDi if divides on days 1-3
All dizygotic twins are DiDi
Monozy twins can be whatever
DiDi: best outcome
See twin peak sign later in pregnancy
Monochorionic / diamniotic
MoDi if divides on days 4-8
See two amniotic sacs, one chorion early on U/S.
Risk TTTS (twin twin transfusion syndrome)
Monochorionic / monoamniotic
MoMo if divides on days 8-13
Risk conjoinment, fetal death 2/2 cord entanglement, etc.
Conjoined
Conjoined if divides on days 13-15
Selective reduction
Can consider selective reduction if triplets or above
Twin-twin transfusion syndrome (TTTS, aka poly-oli sequence)
One small, oligohydramnios, growth restriction, anemia twin (donor), large, plethoric, hypervolemic, cardiac failure, polyhydramnios polycythemic / hydropic twin (recipient)
Dx of TTTS
Dx with ultrasound, historically managed with serial amnioreduction, but now laser coagulation of artery by fetal surgeons improves outcomes.
