Obstetric Issues, Labor, and Delivery
Amniocentesis is a procedure that involves the aspiration of amniotic fluid from the amniotic sac during pregnancy. It is generally carried out with a spinal needle (20–22 gauge) in a transabdominal approach, using a sterile technique under continuous ultrasound guidance. ∗
In Rh and other blood group isoimmunizations, amniocentesis has traditionally been used for bilirubin assessment using ΔOD 450, but it is being done far less frequently now because middle cerebral artery Doppler has been found to be extremely accurate in predicting the degree of fetal anemia. In this setting amniocentesis is used to determine whether the fetus is Rh positive or positive for the sensitized antigen so that testing can be avoided if the fetus is not at risk. ∗
3. What are the complications of amniocentesis?
Miscarriage and fetal loss (less than 0.1%) above the background rate of spontaneous loss (0.5–1%) in specialized centers with high procedure volumes (Eddleman, Towner). The rate is higher in low-volume centers (Tabor).
Transient leakage of amniotic fluid (about 1%)
Persistent rupture of membranes (rare)
Failure to achieve diagnosis (i.e., cell culture failure, which occurs in 1% of cases)
Increased Rhesus isoimmunization, especially if the placenta is transversed. In Rh-negative women, Rh immune globulin (e.g., RhoGAM) is given to prevent sensitization. ∗†‡
5. What options, aside from amniocentesis, are available for prenatal diagnosis?
Available tests for fetal chromosome evaluation are classified as “diagnostic” (the result is a definitive karyotype) or “screening” (the result quantifies the risk of aneuploidy).
Chorionic villus sampling: This is the only alternative to amniocentesis that is considered “diagnostic”; it is performed in the first trimester (9 to 12 weeks). This procedure involves either transvaginal or transabdominal ultrasound-guided needle aspiration of a small amount of placental tissue and can be used for cytogenetic, biochemical, or DNA testing. The procedure-related loss rate is 0.8%.
Preimplantation genetic diagnosis: This is an adjunct to in vitro fertilization. One or more cells are removed from the developing embryo 2 to 4 days after fertilization and then analyzed. Only normal embryos are selected for implantation. When the parents are carriers of an adverse genetic trait, it may obviate the need for testing during pregnancy. It is not considered “diagnostic” for karyotype, however, because of the high rate of mosaicism.
Fetal free DNA screening from maternal blood: This is considered an “advanced screening test” because of very high sensitivity and specificity (>99%) for trisomy 21 and other common aneuploidies. Introduced in late 2011, this testing is currently very expensive and recommended only for women who have one or more risk factors for aneuploidy (based on maternal serum screening, ultrasound screening, advanced maternal age, family history). In women without risk factors, the positive predictive value is not yet known.
Second-trimester ultrasound: Many structural fetal defects (e.g., anencephaly, omphalocele) can routinely be seen in patients who undergo ultrasound scanning during the second trimester. Other defects, such as major cardiac defects, can be seen most of the time depending on the sophistication of the center, type of equipment, patient body habitus, and other factors. In addition, many fetuses with chromosome abnormalities including trisomy 13, 18, and 21 syndromes will have findings that will lead to subsequent amniocentesis to confirm the diagnosis.
Combinations of first-trimester ultrasound and first-trimester or second-trimester maternal serum screening: These screening tests involve ultrasound evaluation of nuchal translucency at 11 to 14 weeks’ gestation, maternal serum levels of human chorionic gonadotropin (hCG) and pregnancy-associated plasma protein A (PAPP-A) at 10 to 14 weeks’ gestation, and “triple
marker” (alpha-fetoprotein (AFP), hCG, estriol) or “quadruple marker” (triple marker plus inhibin-A) at 15 to 20 weeks’ gestation. Depending on which combination of tests is performed, detection of Down syndrome is 60% to 95% with a 5% screen positive rate. Reasonable detection rates are also achieved for trisomy 18 and open neural tube defects. ∗†‡§¶∗∗††
Third-trimester hemorrhage refers to any bleeding from the genital tract during the third trimester of pregnancy. In practice, it refers to any bleeding that occurs from the time of viability, (i.e., 23 to 24 weeks’ gestation). The common causes are classified as placenta previa (7%), placental abruption (13%), and other bleeding (80%), including local lesions of the lower genital tract, vasa previa, early labor, trauma, neoplasia, and marginal placental separation. Such bleeding complicates about 6% of pregnancies. ∗
Ultrasound visualization is the method of choice for diagnosis of placenta previa. Multiple reports show a transvaginal approach to be safe and superior in its accuracy compared with transabdominal ultrasound. ∗
9. How is placenta previa classified?
Complete: The placenta symmetrically covers the entire internal os of the cervix.
Partial: The placenta lies asymmetrically toward one wall of the uterus and crosses part of the internal os.
Marginal: The placental edge just reaches the edge of the internal cervical os.
Low-lying placenta: Placental edge is within 2 centimeters of the internal os.
12. What are the complications of placenta previa?
Hemorrhage in third trimester, possibly catastrophic: Uterine contractions, cervical shortening/dilation, and sexual intercourse are common triggers for hemorrhage.
Preterm delivery: 50%—the vast majority of increased perinatal mortality with placenta previa is caused by prematurity.
Placenta accreta: when the placenta infiltrates the uterine wall (1% to 5%; 25% with one previous uterine surgery; 45% if more than one previous surgery)
Increased risk of postpartum hemorrhage
Fetal growth restriction: Studies are inconsistent, and the majority show no increased rates of IUGR with placenta previa
Placental abruption is the separation of the normally implanted placenta before the birth of the fetus. It results from bleeding from a small arterial vessel into the decidua basalis. It is termed a revealed abruption when vaginal bleeding is present (90%) and a concealed abruption if no bleeding is visible (10%). It is uniquely dangerous to the fetus and the mother because of its serious pathophysiologic sequelae. The incidence varies but averages about 0.83% or 1 in 120 deliveries. Abruption severe enough to cause fetal death is less common (approximately 1 in 420 deliveries). ∗†
14. What are the main risk factors for a placental abruption? Is placental abruption a recurrent disease?
Maternal mortality: less than 1%
Disseminated intravascular coagulation
Severe Rhesus isoimmunization: occurs in Rh-negative mothers unless there is adequate treatment with anti-D immunoglobulin
Fetal and neonatal complications
IUGR: especially in preterm deliveries
Increased risk of congenital malformations: 4.4%
Greater incidence of abnormal neurodevelopment at 2 years
Perinatal mortality: 14.4 to 67% higher rates occur at earlier gestations; high rate of stillbirth, fetal distress, and asphyxia. Most mortality is caused by prematurity
Fetomaternal hemorrhage with resultant fetal anemia: more common in abruption associated with maternal trauma
Fetomaternal hemorrhage is caused by a disruption of the normal barrier at the placental-decidual interface. It may occur with abruptio placentae; however, it occurs more commonly with abruptio placentae associated with maternal trauma, with maternal trauma without abruptio placentae, or spontaneously without an apparent precipitating event. Approximately 5% of stillbirths without apparent cause are the result of fetomaternal hemorrhage. The diagnosis is made by performing a Kleihauer–Betke test on maternal blood, which allows quantification of fetal cells in maternal serum. In patients with spontaneous fetomaternal hemorrhage, the presenting symptom is decreased fetal movement. If the fetus is still alive and the hemorrhage is severe enough, the diagnosis is often made because of a sinusoidal fetal heart rate (FHR) tracing. Treatment can consist of immediate delivery if the fetus is near term or intrauterine transfusion if the fetus is premature and no abruption is apparent. ∗
17. A 32-year-old, G2P1001 woman at term gestation presents in labor. Her membranes are intact, she is afebrile, and the fetal heart tracing is reassuring. Reviewing her prenatal records, you notice that she had a positive Group B streptococcal culture obtained at 34 weeks’ gestation. She is allergic to penicillin and “had difficulty breathing and swelled up” when she received it many years ago. What therapy is appropriate?
For pencillin-allergic women with high risk of anaphylaxis (as in the present case), the CDC’s 2010 guidelines recommend susceptibility testing against both erythromycin and clindamycin. Prophylaxis with erythromycin is no longer recommended, even if sensitivity is documented. Prophylaxis with clindamycin is recommended if GBS is proved sensitive to both clindamycin and erythromycin and if there is no inducible resistance to clindamycin using D-zone testing. If sensitivity is unknown, or if all these requirements are not met, vancomycin is recommended. ∗†‡
18. What are the major risk factors for preterm labor?
Preterm premature rupture of membranes
Maternal age younger than 18 years
Diethylstilbestrol (DES) exposure