High-Risk Pregnancies
Kristen R. Suhrie, Sammy M. Tabbah
The care of high-risk pregnancies should be coordinated with an experienced maternal-fetal medicine specialist.
In general, high-risk pregnancies are those that increase the likelihood of maternal complications, miscarriage, fetal death, preterm delivery, intrauterine growth restriction (IUGR), poor cardiopulmonary or metabolic transitioning at birth, fetal or neonatal disease, congenital malformations, or intellectual impairment and other handicaps (Table 114.1 ).There is no accepted comprehensive definition of what constitutes a high-risk pregnancy , therefore, specific epidemiologic data regarding the incidence/prevalence cannot be reliably reported. Some factors, such as ingestion of a teratogenic drug in the first trimester, are causally related to the risk, while others, such as polyhydramnios, are associations that alert a physician to determine the etiology and avoid the inherent risks associated with excessive amniotic fluid. Although assessing antepartum risk is important in reducing perinatal mortality and morbidity, some pregnancies become high risk only during labor and delivery; therefore careful monitoring is critical throughout the intrapartum course.
Table 114.1
Factors Associated With High-Risk Pregnancy
| ECONOMIC |
| CULTURAL/BEHAVIORAL |
| BIOLOGIC/GENETIC |
| REPRODUCTIVE |
| MEDICAL |
Identifying high-risk pregnancies is important not only because it is the first step toward prevention but also because critical steps may often be taken to reduce the risks to the fetus or neonate if the physician is alerted to the specific condition early in pregnancy.
Genetic Factors
The occurrence of chromosomal abnormalities, congenital anomalies, inborn errors of metabolism, cognitive delay, or any familial disease in blood relatives increases the risk of the same condition in the infant. Because many parents recognize only obvious clinical manifestations of genetically determined diseases, specific inquiry should be made about any disease affecting one or more blood relatives. A high index of suspicion should be maintained to the possibility of autosomal recessive disorders in offspring of couples who are closely related (i.e., consanguinity).
Maternal Factors
The lowest neonatal mortality rate occurs in infants of mothers who receive adequate prenatal care and who are 20-30 yr of age. Pregnancies in both teenagers and women older than 40, particularly primiparous women, are at increased risk for IUGR, fetal distress, preeclampsia, and stillbirth. Advanced maternal age increases the risk of both chromosomal and nonchromosomal fetal malformations (Fig. 114.1 ).
Maternal illness (Table 114.2 ), multiple pregnancies (particularly those involving monochorionic twins), infections (Table 114.3 ), and certain drugs (see Chapter 115.4 ) increase the risk for the fetus. The use of assisted reproductive technology (e.g., ovulation induction, in vitro fertilization, intracytoplasmic sperm injection) increases the risk of prematurity, perinatal mortality, infant morbidity, low and very-low birthweight, imprinting disorders, and cerebral palsy. These risks are largely because of the increase in multiple gestations with such technology and the association with prematurity . The risks for birth defects are also increased with assisted reproductive technology, in part because of epigenetic effects on gene expression.
Table 114.2
Maternal Conditions Affecting the Fetus or Neonate
| DISORDER | EFFECT(S) | MECHANISM(S) |
|---|---|---|
| Assisted reproductive technology | Beckwith-Wiedemann, Silver-Russel, Angelman syndromes | Altered imprinting |
| Autoantibody against folate receptors | Neural tube defects | Blockage of cellular uptake of folate |
| Cervical neoplasia | Preterm premature rupture of membranes, preterm birth | Associated with loop electrosurgical excision procedure or cone therapy |
| Cholestasis | Preterm delivery, intrauterine fetal demise | Unknown, possibly bile acid–induced fetal arrhythmia |
| Cyanotic heart disease | IUGR | Low fetal oxygen delivery |
| Diabetes mellitus: | ||
| Mild | LGA, hypoglycemia | Fetal hyperglycemia: produces hyperinsulinemia; insulin promotes growth |
| Severe | Growth restriction | Vascular disease, placental insufficiency |
| Drug addiction | IUGR, neonatal withdrawal | Direct drug effect plus poor nutrition |
| Endemic goiter | Hypothyroidism | Iodine deficiency |
| Graves' disease | Transient neonatal thyrotoxicosis | Transplacental passage of IgG thyroid-stimulating antibody |
| Herpes gestationis (noninfectious) | Bullous rash, intrauterine fetal demise | Autoantibody similar to that in bullous pemphigoid |
| Hyperparathyroidism | Neonatal hypocalcemia | Maternal calcium crosses to fetus and suppresses fetal parathyroid gland |
| Hypertension | IUGR, intrauterine fetal demise | Placental insufficiency, fetal hypoxia |
| Idiopathic thrombocytopenic purpura | Thrombocytopenia | Nonspecific maternal platelet antibodies cross placenta |
| Isoimmune neutropenia or thrombocytopenia | Neutropenia or thrombocytopenia | Specific antifetus neutrophil or platelet antibody crosses placenta after sensitization of mother |
| Malignant melanoma | Placental or fetal tumor | Placental metastasis |
| Myasthenia gravis | Transient neonatal myasthenia | IgG antibody to acetylcholine receptor crosses placenta |
| Myotonic dystrophy | Neonatal myotonic dystrophy, congenital contractures, respiratory insufficiency | Genetic anticipation |
| NMDAR antibody encephalitis | Cortical dysplasia | Transplacental antibody |
| Obesity | LGA or IUGR, hypoglycemia | Unknown, similarities to diabetes |
| Phenylketonuria | Microcephaly, retardation | Elevated fetal phenylalanine values |
| Poor nutrition | IUGR, adult insulin resistance | Reduced fetal nutrients, nutritional programming |
| Preeclampsia, eclampsia | IUGR, thrombocytopenia, neutropenia, fetal demise | Uteroplacental insufficiency, fetal hypoxia, vasoconstriction |
| Renal transplantation | IUGR | Uteroplacental insufficiency |
| Rhesus or other blood group sensitization | Fetal anemia, hypoalbuminemia, hydrops, neonatal jaundice | IgG crosses placenta and is directed to fetal cells with antigen |
| Sickle cell anemia | Preterm birth, IUGR, stillbirth | Placental insufficiency via maternal sickling, producing fetal hypoxia |
| Systemic lupus erythematosus | Congenital heart block, rash, anemia, thrombocytopenia, neutropenia | Antibody directed to fetal heart, red and white blood cells, and platelets |
IgG, Immunoglobulin G; LGA, large for gestational age; NMDAR, antibody to N -methyl-D -aspartate receptor; IUGR, intrauterine growth restriction.
Table 114.3
Maternal Infections Affecting the Fetus or Newborn
| INFECTION | MODE(S) OF TRANSMISSION | NEONATAL OUTCOME |
|---|---|---|
| BACTERIA | ||
| Group B streptococcus | Ascending cervical | Sepsis, pneumonia |
| Escherichia coli | Ascending cervical | Sepsis, pneumonia |
| Listeria monocytogenes | Transplacental | Sepsis, pneumonia |
| Mycoplasma hominis | Ascending cervical | Pneumonia |
| Chlamydia trachomatis | Vaginal passage | Conjunctivitis, pneumonia |
| Syphilis | Transplacental, vaginal passage | Congenital syphilis |
| Neisseria gonorrhoeae | Vaginal passage | Ophthalmia (conjunctivitis), sepsis, meningitis |
| Mycobacterium tuberculosis | Transplacental | Prematurity, fetal demise, congenital tuberculosis |
| VIRUS | ||
| Rubella | Transplacental | Congenital rubella |
| Cytomegalovirus | Transplacental, breast milk (rare) | Congenital cytomegalovirus or asymptomatic |
| HIV | Transplacental, vaginal passage, breast milk | Congenital or acquired immunodeficiency syndrome |
| Hepatitis B | Vaginal passage, transplacental, breast milk | Neonatal hepatitis, chronic hepatitis B surface antigen carrier state |
| Hepatitis C | Transplacental and vaginal passage | Rarely neonatal hepatitis, ~5% chronic carrier state possible |
| Herpes simplex type 2 or 1 | Intrapartum exposure | Neonatal herpes simplex virus |
| Neonatal encephalitis; disseminated viremia, or cutaneous infection | ||
| Varicella-zoster | Transplacental: | |
| Early | Congenital anomalies | |
| Late | Neonatal varicella | |
| Parvovirus | Transplacental | Fetal anemia, hydrops |
| Coxsackievirus B | Fecal-oral | Myocarditis, meningitis, hepatitis |
| Rubeola | Transplacental | Abortion, fetal measles |
| West Nile |
Transplacental (rare) Possible perinatal |
Uncertain, possible rash, encephalitis |
| Zika | Transplacental | Congenital microcephaly, intracranial calcifications, brain abnormalities, retinal lesions |
| Chikungunya | Transplacental (rare), perinatal | Neonatal encephalitis |
| Dengue | Transplacental, perinatal | Neonatal sepsis-like symptoms |
| PARASITES | ||
| Toxoplasmosis | Transplacental | Congenital toxoplasmosis |
| Malaria | Transplacental | Abortion, prematurity, intrauterine growth restriction |
| FUNGI | ||
| Candida | Ascending, cervical | Sepsis, pneumonia, rash |
Preterm birth is common in high-risk pregnancies (see Chapter 117 ). Factors associated with prematurity (see Table 114.1 ) include multiple gestations as well as biologic markers such as cervical shortening, genital infection, presence of fetal fibronectin in cervicovaginal secretions, serum α-fetoprotein (AFP), and premature rupture of membranes (PROM). PROM occurs in 3% of all pregnancies in the United States and is a leading identifiable cause of prematurity.
The presence of polyhydramnios or oligohydramnios indicates high-risk pregnancies. Amniotic fluid volume is variable throughout pregnancy and progressively increases from 10 to 30 wk of gestation. On average, volume is typically <10 mL at 8 wk and increases to 630 and 770 mL at 22 and 28 wk, respectively. After 30 wk, the rate of increase slows and the volume remains fairly constant until 36-38 wk gestation. This is followed by a progressive decline, with an average volume of 515 mL at 41 wk of gestation. Polyhydramnios complicates 1–3%, and oligohydramnios 1–5%, of pregnancies; although the true incidence of amniotic fluid disorders is confounded by the lack of a uniform approach to diagnosis. The ultrasound (US) criteria for these diagnoses are based on either the amniotic fluid index (AFI) or a deepest vertical pocket (DVP). The AFI is determined by measuring the vertical dimension of amniotic fluid pockets in 4 quadrants and reporting the sum of these values. An index >24 cm suggests polyhydramnios, whereas an index <5 cm suggests oligohydramnios. The DVP method reports the deepest pocket of fluid identified with a value of 2-8 cm is considered normal.
Polyhydramnios is associated with preterm labor, abruptio placentae, maternal diabetes, multiple congenital anomalies, aneuploidy, and fetal neuromuscular dysfunction or obstruction of the gastrointestinal tract that interferes with reabsorption of the amniotic fluid that is normally swallowed by the fetus (Table 114.4 ). Increased fetal urination, as with congenital nephrotic syndrome, or edema formation, such as hydrops fetalis, is also associated with excessive amniotic fluid volume. US demonstrates the increased amniotic fluid surrounding the fetus and detects associated fetal anomalies, hydrops, pleural effusions, and ascites. Idiopathic polyhydramnios is the most common cause, affecting approximately 40% of patients. About 25% of these cases will demonstrate an abnormality in the postnatal period. Otherwise, approximately 33% of prenatally detected cases have an associated anomaly, and 25% are associated with maternal diabetes. Severe and symptomatic polyhydramnios may be managed by serial reduction amniocenteses. Treatment is indicated for acute maternal respiratory discomfort and threatened preterm labor, or to provide time for the administration of corticosteroids to enhance fetal lung maturity.
Table 114.4
Conditions Associated With Disorders of Amniotic Fluid Volume
| OLIGOHYDRAMNIOS |
| POLYHYDRAMNIOS |
| Congenital Anomalies |
| Syndromes |
|
TORCH* |
| Other |
* Toxoplasmosis, other agents, rubella, cytomegalovirus, and herpes simplex.
CNS, Central nervous system; GU, genitourinary.
Oligohydramnios is associated with congenital anomalies; IUGR; severe renal, bladder, or urethral anomalies; and drugs that interfere with fetal urination (see Table 114.4 ). Oligohydramnios becomes most evident after 16-20 wk of gestation, when fetal urination is the major source of amniotic fluid. PROM is a common cause of oligohydramnios and must be ruled out if present, especially if a normal-sized bladder and kidneys are seen on fetal US. Oligohydramnios causes fetal compression abnormalities such as fetal distress/stillbirth from umbilical cord compression, clubfoot, spadelike hands, and a flattened nasal bridge. The most serious complication of chronic oligohydramnios is pulmonary hypoplasia , especially if present during the canalicular stage of fetal lung development, which occurs between 16 and 24 wk of gestation. The risk of umbilical cord compression during labor and delivery is increased in pregnancies complicated by oligohydramnios and may be alleviated by saline amnioinfusion via a transcervical intrauterine pressure catheter, which has been demonstrated to reduce the need for cesarean section and improve Apgar scores.
A pregnancy should be considered high risk when the uterus is inappropriately large or small. A uterus large for the estimated stage of gestation suggests the presence of multiple fetuses, polyhydramnios, or an excessively large infant. An inappropriately small uterus suggests oligohydramnios or poor fetal growth.
Mode of delivery is influenced by a complex interplay between maternal-fetal factors. Spontaneous vaginal delivery is always preferred when not otherwise contraindicated. Operative vaginal delivery with vacuum or forceps is a safe alternative to cesarean delivery in appropriately selected patients. The absolute rate of significant newborn injury from these procedures is low, with rates ranging from 1 in 650-850 for intracranial hemorrhage and 1 in 220-385 for neurologic complications . With some of these injuries, the indication for operative vaginal delivery is more likely to be associated with the injury than the procedure itself, and could not have been prevented with a cesarean birth.
Cesarean delivery is indicated for a wide variety of circumstances. Cesarean-born infants present problems that are often related to the unfavorable obstetric circumstance that necessitated the operation. In normal term pregnancies without indication of fetal distress, cesarean delivery carries a greater neonatal risk than delivery through the birth canal. Even when accounting for gestational age, any malformations, birthweight, and multiple gestations, infants born ≥34 wk of gestation via elective cesarean section have 2 times the mortality rate of babies born following a planned vaginal birth, even if cesarean delivery was ultimately required. They also are 1.4 times as likely to require neonatal intensive care unit (NICU) admission and 1.8 times as likely to require breathing support for >30 min after birth. Cesarean-born infants are also at increased risk for persistent pulmonary hypertension of the newborn . An elective cesarean birth should be delayed until ≥39 wk of gestation, assuming there is no indication for delivery earlier.
Obstetric anesthesia is a vital component of care on the labor and delivery unit. The most common form of anesthesia in this patient population is regional (i.e., epidural or spinal). From the fetal/neonatal standpoint, the most significant complication encountered with this procedure is acute maternal hypotension, which can significantly impair uteroplacental perfusion. Fetal heart rate (FHR) abnormalities are common in this circumstance and, rarely, require emergent cesarean delivery if not amenable to standard in utero resuscitative efforts. Opioid analgesia is sometimes used in women who are not candidates for regional anesthesia. This form of pain relief is best avoided as delivery approaches, to minimize risk of neonatal depression. To this end, when opioid use is necessary, it is best to prescribe regimens that have a very short half-life. It is essential that the pediatric team is present at the birth in women receiving opioid analgesia. Furthermore, the pediatricians must be alerted to the specific type of opioid used, because all these drugs cross the placenta and have varying neonatal pharmacokinetics. Some of the common regimens used and their respective neonatal half-life are listed in the referenced American College of Obstetricians and Gynecologists (ACOG) practice bulletin on obstetric anesthesia.