Fetal Complications of Pregnancy

• Small for gestational age (SGA)


  Newborns with birth weight less than the 10th percentile
• Large for gestational age (LGA)


  Newborns with birth weight greater than the 90th percentile
• Symmetric SGA


  • Fetus is proportionally small
• Asymmetric SGA


  • Certain organs of the fetus are disproportionately small, with the skull at a greater percentile than the rest of the body
• Screening for disorders of fetal growth

  1. Uterine fundal height (in cm) should be approximately equal to the gestational age (in weeks)

  2. If fundal height varies by more than 3 cm from the gestational age, ultrasound is usually obtained
• Birth percentiles are useful in identifying small neonates, but fail to distinguish between infants who reached their growth potential and those with disproportionate growth
• Regulation of fetal growth

  1. Placental cytotrophoblast villi anchor to the uterine decidua

  2. Vascular connections form between the maternal circulation and the intervillous spaces, enabling endocrine and paracrine signaling

  3. Placental growth is supported by increased substrate delivery and perfusion
• The ultimate growth potential of the fetus is felt to be predetermined genetically
• Factors that can result in infants being SGA

  • Decreased growth potential
  • Intrauterine growth restriction (IUGR)
• Causes of decreased growth potential

  • Congenital abnormalities
  • Intrauterine infections
  • Teratogen exposure
  • Substance abuse
  • Small maternal stature
  • Pregnancy at high altitudes
  • Female fetus
• Causes of intrauterine growth restriction (IUGR)

  • Maternal factors including hypertension, anemia, chronic renal disease, malnutrition, and severe diabetes
  • Placental factors including placenta previa, chronic abruption, placental infarction, multiple gestations
• Diagnosis of SGA


  1. Fundal height measurement at each prenatal visit

  2. If fundal height is 3 cm less than expected, fetal growth should be estimated via ultrasound

  3. Differentiate IUGR fetuses using Doppler investigation of the umbilical artery
• Treatment of SGA


  1. Explore underlying etiology

  2. Treat with low-dose aspirin, heparin, and corticosteroids in some cases

  3. Deliver if fetal testing is nonreassuring
• Macrosomia


  Birth weight greater than 4,500 g
• Risks of macrosomia


  • Higher risk of shoulder dystocia and birth trauma with vaginal deliveries
  • Increased risk for childhood leukemia, Wilms tumor, and osteosarcoma
  • Increased risk of cesarean delivery, perineal trauma, and postpartum hemorrhage for mothers
• Risk factors for fetal macrosomia

  • Preexisting or gestational diabetes mellitus
  • Maternal obesity
  • Increased maternal weight gain in pregnancy
  • Previous delivery of an LGA infant
  • Postterm pregnancy
  • Multiparity
  • Advanced maternal age
• Diagnosis of macrosomia


  1. Fundal height greater than expected

  2. Leopold's examination reveals a large fetus

  3. Ultrasound for estimated fetal weight, but accuracy is limited beyond the 90th percentile
• Clinicians are obligated to offer elective cesarean delivery for estimated fetal weight of 5,000 g or greater in women without gestational diabetes, and 4,500 g or greater in women with gestational diabetes
• Postterm pregnancies


  • Have an increased rate of macrosomic infants
  • Multiparity and advanced maternal age are also risk factors, but these are mostly secondary to the increased prevalence of diabetes and obesity
• Risk factors for macrosomic infants

  • Diabetes
  • Maternal obesity
  • Postterm pregnancy
  • Previous LGA or macrosomic infant
  • Maternal stature
  • Multiparity
  • AMA
  • Male infant
  • Beckwith-Wiedemann syndrome (pancreatic islet cell hyperplasia)
• Prevention of LGA


  • Counseling women about the goals for gestational weight gain including specific counseling about diet and exercise in pregnancy
  • Tight control of blood glucose during pregnancy for women with type 1 and 2 pregestational diabetes or gestational diabetes
• Maternal obesity


  • An independent risk factor for LGA infants
  • Obese patients must be encouraged to lose weight before conception and offered specific programs to help them do so
  • Once pregnant, these patients should be advised to gain less weight (but never to lose weight) than the average patient, and they should be referred to a nutritionist for assistance in maintaining adequate nutrition, with some control of caloric intake
• Induction of labor for LGA pregnancies

  1. Used primarily when there is either excellent dating or lung maturity as assessed via amniocentesis

  2. For induction in the setting of an unfavorable cervix, prostaglandins and mechanical means should be used to achieve cervical ripening, and this can often take several days to accomplish
• Prospective studies of the practice of induction for impending macrosomia have not demonstrated an increase in cesarean delivery rates, but do appear to lead to lower rates of macrosomia
• Amniotic fluid volume


  • Reaches its maximum of about 800 mL at about 28 weeks, maintained until close to term when it begins to fall to about 500 mL at week 40
  • Maintained by production of the fetal kidneys and lungs and resorption by fetal swallowing and the interface between the membranes and the placenta
• Amniotic fluid index (AFI)

  • Calculated by dividing the maternal abdomen into quadrants, measuring the largest vertical pocket of fluid in each quadrant in centimeters, and summing them
  • An AFI of less than 5 is considered oligohydramnios
  • An AFI greater than 20 or 25 is used to diagnose polyhydramnios, depending on gestational age
• Oligohydramnios


  • Associated with a 40-fold increase in perinatal mortality
  • Partially because without the amniotic fluid to cushion it, the umbilical cord is more susceptible to compression thus leading to fetal asphyxiation
  • Also associated with congenital anomalies, particularly of the genitourinary system, and growth restriction
  • In labor, nonreactive nonstress tests, fetal heart rate (FHR) decelerations, meconium, and cesarean delivery due to nonreassuring fetal testing are all associated with an AFI of less than 5
• Causes of oligohydramnios


  • Decreased production (chronic uteroplacental insufficiency, congenital abnormalities of the genitourinary tract)
  • Increased withdrawal (rupture of membranes)
• Polyhydramnios


  • Defined by an AFI greater than 20 or 25, present in 2% to 3% of pregnancies
  • Associated with fetal structural and chromosomal abnormalities, maternal diabetes, and malformations such as neural tube defects, obstruction of the fetal alimentary canal, and hydrops
• Causes of polyhydramnios


  • Obstruction of the gastrointestinal tract (e.g., tracheoesophageal fistula, duodenal atresia)
  • Increased levels of circulating glucose in diabetic patients acting as an osmotic diuretic in the fetus
  • Hydrops secondary to high output cardiac failure
  • Monozygotic multiple gestations leading to twin-to-twin transfusion syndrome
• Rh incompatibility and alloimmunization

  • If a woman is Rh negative and her fetus is Rh positive, she may be sensitized to the Rh antigen and develop antibodies
  • These IgG antibodies cross the placenta and cause hemolysis of fetal RBCs, leading to erythroblastosis fetalis or fetal hydrops
• Prevalence of Rh negativity by race and ethnicity

  • Caucasian: 15%
  • African American: 8%
  • African: 4%
  • Native American: 1%
  • Asian: <1%
• RhoGAM


  • A standard dose of 0.3 mg of Rh IgG will eradicate 15 mL of fetal RBCs (30 mL of fetal blood with a hematocrit of 50)
  • This dose is adequate for a routine pregnancy, but may need to be increased in the setting of placental abruption or a large fetomaternal hemorrhage
• Scites


  Fluid accumulation in the body cavities of a fetus
• Pleural effusions


  Fluid accumulation in the chest cavity of a fetus
• RBCs (red blood cells) are cleared by the placenta before birth but can lead to jaundice and neurotoxic effects in the neonate
• Rh-negative patient


  Patient who does not have the Rh antigen on their red blood cells
• Preventing Rh sensitization in an Rh-negative patient

  1. Antibody screen at initial visit

  2. RhoGAM administration at 28 weeks and postpartum if neonate is Rh positive

  3. Additional RhoGAM doses if fetal RBCs exceed 15mL
• Rh sensitized patient


  Rh-negative patient who has developed Rh antibodies
• Managing Rh sensitized patient

  1. Check antibody titer

  2. Serial amniocentesis if titer ≥1:16

  3. Determine fetal Rh status

  4. Screen for fetal anemia using MCA Doppler

  5. Perform PUBS and intrauterine transfusion if fetal anemia