Medical School · Year 2 · Reproductive · includes a quiz and discussion video

Lecture 7: Prenatal Care and Pregnancy Complications

Unit 2.4: Reproductive System

Learning Objectives

By the end of this lecture, students will be able to:

1. Describe the components of routine prenatal care
2. Explain prenatal screening and diagnostic testing
3. Describe the hypertensive disorders of pregnancy
4. Explain gestational diabetes screening and management
5. Describe common pregnancy complications including preterm labor
6. Explain Rh incompatibility and its prevention

Section 1: Routine Prenatal Care - Initial Visit and Ongoing Monitoring

Prenatal care represents a systematic approach to monitoring pregnancy, identifying complications early, and providing education and support to optimize maternal and fetal outcomes. The structure of prenatal care follows established patterns refined over decades of clinical experience.

The initial prenatal visit, ideally occurring in the first trimester, establishes the foundation for pregnancy management. A comprehensive history includes medical conditions that may affect pregnancy (hypertension, diabetes, thyroid disease, seizure disorders), surgical history (particularly uterine surgery), obstetric history using the gravidity and parity system (including prior pregnancy outcomes, complications, delivery modes), family history of genetic conditions, and social history including substance use, domestic safety, and support systems. Accurate pregnancy dating is essential, as many management decisions depend on gestational age. The last menstrual period (LMP) provides an estimated due date using Naegele's rule: subtract three months, add seven days, and add one year. First-trimester ultrasound dating (by crown-rump length) is accurate to within 5-7 days and takes precedence over LMP when discrepant by more than 7 days.

The initial laboratory panel screens for conditions affecting pregnancy management. Blood type and Rh status identify candidates for Rh immunoglobulin. Antibody screening detects alloantibodies that could cause hemolytic disease. Complete blood count identifies anemia. Rubella immunity status determines need for postpartum vaccination. Hepatitis B surface antigen identifies chronic infection requiring neonatal prophylaxis. HIV testing (opt-out approach) enables interventions reducing vertical transmission. Syphilis serology identifies infection requiring treatment. Urinalysis and culture detect asymptomatic bacteriuria, which if untreated progresses to pyelonephritis in 30% of pregnant women.

The visit schedule traditionally follows increasing frequency as pregnancy advances. From initial confirmation through 28 weeks, visits occur every four weeks. From 28 to 36 weeks, visits increase to every two weeks. From 36 weeks until delivery, weekly visits are standard. High-risk pregnancies require individualized, often more frequent, monitoring.

Routine monitoring at each visit includes weight (excessive gain may indicate fluid retention; inadequate gain suggests poor fetal growth), blood pressure (rising values may herald preeclampsia), fundal height (measured in centimeters from the pubic symphysis to the uterine fundus, approximating gestational age in weeks from 20-36 weeks), fetal heart tones (detectable by Doppler after 10-12 weeks), and fetal movement assessment (reported by the mother after 20 weeks).

<image>Panel A: Horizontal timeline from conception to 40 weeks showing visit frequency with monthly visits from confirmation to 28 weeks, biweekly visits from 28-36 weeks, and weekly visits from 36-40 weeks. Panel B: Initial visit assessments including history intake, blood draw (CBC, type/screen, rubella, HBsAg, HIV, syphilis, UA/culture), and dating ultrasound, with routine visit components (blood pressure, weight, fundal height, fetal heart tones). Panel C: Key milestone testing at 28 weeks including glucose challenge test, repeat antibody screen for Rh-negative patients, and Tdap vaccination, with fundal height growth chart showing normal range from 20-40 weeks. Panel D: Naegele's rule calculation with calendar graphic showing LMP date, arithmetic steps (subtract 3 months, add 7 days, add 1 year), and estimated due date determination.</image>

Section 2: Prenatal Screening and Diagnostic Testing

Prenatal screening and diagnostic testing aim to identify fetal chromosomal abnormalities, structural anomalies, and genetic conditions. Understanding the distinction between screening (assessing risk) and diagnosis (confirming condition) is essential for patient counseling.

First-trimester screening, performed between 11-14 weeks, combines ultrasound and biochemical markers. The nuchal translucency, a sonographic measurement of the fluid collection at the posterior fetal neck, is increased in Down syndrome and other aneuploidies; increased NT also correlates with cardiac defects regardless of chromosomal status. Maternal serum markers include pregnancy-associated plasma protein-A (PAPP-A), which is decreased in trisomy 21, and free beta-hCG, which is elevated in trisomy 21. Combined first-trimester screening detects approximately 85% of Down syndrome cases with a 5% false-positive rate.

Second-trimester screening (15-22 weeks) typically involves the quad screen measuring four analytes. Alpha-fetoprotein (AFP) is elevated in neural tube defects (open spina bifida, anencephaly) and abdominal wall defects (gastroschisis, omphalocele); AFP is decreased in Down syndrome. Human chorionic gonadotropin is elevated in Down syndrome. Unconjugated estriol is decreased in Down syndrome. Inhibin A is elevated in Down syndrome. The characteristic pattern for Down syndrome is low AFP, high hCG, low estriol, and high inhibin A. Trisomy 18 shows low levels of all four markers.

Cell-free DNA (cfDNA) screening, also called noninvasive prenatal testing (NIPT), represents a major advance in aneuploidy screening. Placental trophoblast cells release DNA fragments into maternal circulation; by 10 weeks' gestation, this cell-free fetal DNA constitutes approximately 10% of total cell-free DNA in maternal plasma. Next-generation sequencing analyzes the proportion of DNA from each chromosome; excess chromosome 21 material indicates trisomy 21. Sensitivity for Down syndrome exceeds 99% with a false-positive rate under 0.1%. cfDNA also detects trisomies 18 and 13 and sex chromosome aneuploidies. Despite excellent performance, cfDNA remains a screening test; positive results require diagnostic confirmation.

Diagnostic testing provides definitive chromosomal analysis but carries procedural risk. Chorionic villus sampling (CVS), performed at 10-13 weeks, obtains placental tissue via transcervical or transabdominal approaches. Amniocentesis, performed at 15-20 weeks (or later), obtains amniotic fluid containing fetal cells. Both allow karyotyping, chromosomal microarray, and genetic testing. Procedure-related pregnancy loss risk is approximately 0.1-0.3% for amniocentesis and approximately 0.5-1% for CVS. Indications include positive screening tests, advanced maternal age, family history of genetic conditions, prior affected pregnancy, and ultrasound abnormalities.

The anatomy ultrasound at 18-22 weeks systematically evaluates fetal structures including brain, spine, heart, abdominal organs, limbs, and placental location.

<image>Panel A: First trimester screening (11-14 weeks) with ultrasound showing nuchal translucency measurement, PAPP-A and free beta-hCG test tubes with detection and false positive rates, and cfDNA panel (10+ weeks) with DNA helix and sequencing chromatogram. Panel B: Second trimester quad screen (15-22 weeks) showing AFP, hCG, estriol, and inhibin A, with interpretation table for Down syndrome (AFP down, hCG up, estriol down, inhibin A up), neural tube defect (AFP markedly elevated), and trisomy 18 (all low). Panel C: CVS procedure (10-13 weeks) showing transcervical catheter approach to placenta under ultrasound guidance with miscarriage risk listed, and amniocentesis (15-20 weeks) showing needle traversing abdominal wall to amniotic cavity. Panel D: Diagnostic results showing karyotype image, chromosomal microarray output, and definitive diagnosis label, distinguishing screening (risk assessment) from diagnosis (confirmation).</image>

Section 3: Hypertensive Disorders of Pregnancy - Classification and Preeclampsia

Hypertensive disorders complicate approximately 10% of pregnancies and represent a leading cause of maternal morbidity and mortality worldwide. Accurate classification guides management and prognosis.

Chronic hypertension is blood pressure ≥140/90 mmHg documented before pregnancy, before 20 weeks' gestation, or persisting beyond 12 weeks postpartum. Management involves continuing or initiating antihypertensive therapy (labetalol, nifedipine, and methyldopa are commonly used; ACE inhibitors and angiotensin receptor blockers are contraindicated due to teratogenicity) with a goal of <140/90, careful surveillance for superimposed preeclampsia, and low-dose aspirin for preeclampsia prevention.

Gestational hypertension is new-onset hypertension ≥140/90 mmHg after 20 weeks' gestation without proteinuria or other features of preeclampsia. While outcomes are generally favorable, approximately 25-50% of women with gestational hypertension ultimately develop preeclampsia, necessitating close monitoring.

Preeclampsia is defined as hypertension ≥140/90 mmHg after 20 weeks' gestation combined with proteinuria (≥300 mg/24 hours, or protein:creatinine ratio ≥0.3, or urine dipstick ≥2+) OR, in the absence of proteinuria, new-onset end-organ dysfunction. The pathophysiology involves abnormal placentation: inadequate trophoblast invasion of spiral arteries leaves them as narrow, high-resistance vessels rather than the dilated, low-resistance channels required for adequate uteroplacental perfusion. Placental ischemia releases anti-angiogenic factors (soluble fms-like tyrosine kinase-1, soluble endoglin) that cause widespread maternal endothelial dysfunction, producing the clinical syndrome of hypertension, proteinuria, and end-organ damage.

End-organ manifestations that define preeclampsia in the absence of proteinuria include renal insufficiency (creatinine >1.1 mg/dL or doubling of baseline), hepatic involvement (transaminases >2× normal), thrombocytopenia (<100,000/μL), pulmonary edema, and cerebral or visual symptoms (headache, visual changes).

Preeclampsia with severe features carries significantly higher risk and is diagnosed by any of the following: blood pressure ≥160/110 mmHg on two occasions, thrombocytopenia <100,000/μL, liver transaminases >2× normal with or without right upper quadrant pain, renal insufficiency, pulmonary edema, or new-onset cerebral or visual disturbances. The presence of severe features changes management, typically mandating delivery.

HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets) represents a severe variant of preeclampsia. Microangiopathic hemolytic anemia produces schistocytes on peripheral smear, elevated LDH, elevated indirect bilirubin, and decreased haptoglobin. Liver involvement causes transaminase elevation and may progress to subcapsular hematoma or hepatic rupture. Thrombocytopenia results from platelet consumption at sites of endothelial damage. HELLP may occur without significant hypertension or proteinuria, making recognition challenging.

<image>Panel A: Four-box classification of hypertensive disorders showing chronic hypertension (before 20 weeks), gestational hypertension (after 20 weeks without proteinuria), preeclampsia (hypertension plus proteinuria or end-organ dysfunction), and eclampsia (preeclampsia plus seizures). Panel B: Preeclampsia pathophysiology with placental bed cross-section comparing normal spiral artery remodeling (wide, dilated) versus preeclampsia (narrow, unremodeled with ischemic placenta), leading to circulating anti-angiogenic factors (sFlt-1, sEng) and maternal endothelial dysfunction. Panel C: Target organ damage radiating outward showing brain (headache, seizures), kidney (proteinuria, glomerular endotheliosis), liver (transaminitis, RUQ pain), and blood (thrombocytopenia, hemolysis with schistocytes). Panel D: HELLP syndrome triad with microangiopathic smear showing fragmented RBCs (Hemolysis), liver with elevated enzyme graph (Elevated Liver enzymes), and platelet count dropping below 100,000 (Low Platelets).</image>

Section 4: Preeclampsia Management and Eclampsia

Management of preeclampsia balances maternal safety against fetal maturity, recognizing that delivery is the only definitive cure. The timing and mode of delivery depend on gestational age and disease severity.

For preeclampsia without severe features at ≥37 weeks' gestation, delivery is recommended. For preeclampsia without severe features at <37 weeks, expectant management with close maternal and fetal surveillance may be considered, with delivery at 37 weeks or earlier if disease progresses or maternal/fetal status deteriorates. Monitoring includes serial blood pressure measurements, twice-weekly laboratory assessment (CBC, creatinine, liver enzymes), and fetal surveillance (non-stress tests, biophysical profiles, growth ultrasounds).

Preeclampsia with severe features generally mandates delivery after maternal stabilization. At ≥34 weeks' gestation, delivery proceeds after stabilization regardless of severe features. Between 24-34 weeks, administration of corticosteroids for fetal lung maturation takes priority, with delivery after the 48-hour steroid course unless maternal or fetal status mandates immediate delivery. Before 24 weeks (previability), delivery is generally recommended given maternal risk and poor neonatal outcomes.

Antihypertensive therapy for acute severe hypertension (≥160/110 mmHg) aims to reduce stroke risk while maintaining uteroplacental perfusion. First-line agents include intravenous labetalol (initial 20 mg bolus, escalating doses), intravenous hydralazine (5 mg boluses), and oral immediate-release nifedipine (10 mg). The goal is blood pressure 140-150/90-100 mmHg; excessive reduction may compromise uteroplacental blood flow.

Magnesium sulfate is the cornerstone of seizure prophylaxis and treatment. For preeclampsia with severe features and for all cases of eclampsia, magnesium sulfate is administered as a 4-6 gram loading dose followed by 1-2 grams/hour maintenance infusion. Magnesium acts at the neuromuscular junction and has vasodilatory effects. Therapeutic serum levels are 4-7 mEq/L. Toxicity follows a predictable sequence: loss of deep tendon reflexes at 8-10 mEq/L, respiratory depression at 12-15 mEq/L, and cardiac arrest at 25-30 mEq/L. Monitoring includes hourly urine output, periodic DTR assessment, and respiratory status. Calcium gluconate is the antidote for magnesium toxicity.

Eclampsia is the occurrence of generalized tonic-clonic seizures in a preeclamptic patient without other identifiable cause. Management includes supportive care (positioning, airway protection, oxygen), magnesium sulfate administration (or bolus if already on magnesium), control of severe hypertension, and delivery planning once the mother is stabilized. Most eclamptic seizures are self-limited; benzodiazepines are reserved for refractory seizures.

<image>Panel A: Decision flowchart by gestational age showing 37+ weeks leading to delivery, 34-37 weeks with severe features leading to stabilize then deliver, less than 34 weeks leading to corticosteroids for 48 hours then delivery, and preeclampsia without severe features under 37 weeks leading to expectant management with surveillance (BP, labs, NST, ultrasound). Panel B: Antihypertensive options for acute severe hypertension including labetalol IV with escalating dose schedule, hydralazine IV, and nifedipine PO, with target BP range 140-150/90-100. Panel C: Magnesium sulfate protocol showing loading dose 4-6g IV, maintenance 1-2 g/hr, therapeutic level 4-7 mEq/L, toxicity ladder (loss of reflexes 8-10, respiratory depression 12-15, cardiac arrest 25-30), monitoring checklist (urine output, DTRs, respiratory rate), and calcium gluconate antidote. Panel D: Eclampsia management showing tonic-clonic seizure posture with steps to protect airway, administer Mg bolus, control blood pressure, and plan delivery.</image>

Section 5: Gestational Diabetes Mellitus

Gestational diabetes mellitus (GDM) is defined as glucose intolerance with onset or first recognition during pregnancy. It complicates approximately 6-9% of pregnancies in the United States, with higher prevalence in certain ethnic groups and those with obesity.

The pathophysiology reflects the normal metabolic adaptations of pregnancy. Placental hormones, particularly human placental lactogen, create progressive insulin resistance to ensure glucose availability for the fetus. In women with adequate pancreatic reserve, increased insulin secretion compensates. GDM develops when insulin secretion cannot match the insulin resistance, resulting in hyperglycemia.

Universal screening occurs at 24-28 weeks' gestation, when placental hormones create maximal insulin resistance. Earlier screening (at initial visit) is indicated for women with risk factors: obesity, prior GDM, prior macrosomic infant, first-degree relative with diabetes, polycystic ovary syndrome, or high-risk ethnicity.

Two screening strategies are used. The one-step approach uses a 75-gram oral glucose tolerance test with fasting, 1-hour, and 2-hour glucose measurements; GDM is diagnosed if any one value is elevated (fasting ≥92, 1-hour ≥180, 2-hour ≥153 mg/dL by IADPSG criteria). The two-step approach, more common in the United States, begins with a non-fasting 50-gram glucose challenge test; if the 1-hour glucose is ≥130-140 mg/dL, the patient proceeds to a fasting 100-gram oral glucose tolerance test. GDM is diagnosed by the Carpenter-Coustan criteria if two or more values are elevated: fasting ≥95, 1-hour ≥180, 2-hour ≥155, 3-hour ≥140 mg/dL.

Complications of GDM affect both mother and fetus. Maternal risks include cesarean delivery (due to macrosomia), preeclampsia, and substantially increased risk of developing type 2 diabetes in the years following pregnancy (approximately 50% by 10 years). Fetal and neonatal risks include macrosomia (birth weight >4000g or >90th percentile), birth injury (shoulder dystocia with associated brachial plexus injury and clavicle fracture), neonatal hypoglycemia (the neonatal pancreas, hyperplastic from intrauterine hyperglycemia, continues secreting high insulin after delivery when maternal glucose supply is cut), hyperbilirubinemia, polycythemia, and respiratory distress syndrome.

Management begins with medical nutrition therapy: carbohydrate counting, distributing carbohydrates throughout the day, and avoiding simple sugars. Moderate exercise improves insulin sensitivity. Glucose self-monitoring guides therapy: fasting targets are <95 mg/dL, 1-hour postprandial <140 mg/dL, and 2-hour postprandial <120 mg/dL.

When diet and exercise fail to achieve targets, pharmacotherapy is indicated. Insulin is the preferred agent as it does not cross the placenta. Metformin and glyburide are alternative oral agents, though both cross the placenta to varying degrees. Fetal surveillance includes growth ultrasounds to detect macrosomia and antepartum testing in later pregnancy. Delivery timing for diet-controlled GDM is at 39-40 weeks; medication-requiring GDM may warrant delivery at 39 weeks.

<image>Panel A: Screening algorithm showing universal screening at 24-28 weeks with two-step pathway (50g GCT then 100g OGTT with Carpenter-Coustan thresholds) and one-step pathway (75g OGTT with IADPSG thresholds), plus early screening for women with risk factors. Panel B: Pathophysiology showing placenta producing hPL and hormones causing insulin resistance in maternal tissues, pancreas with inadequate compensation, and resulting hyperglycemia. Panel C: Complications showing maternal risks (cesarean delivery, preeclampsia, future T2DM with timeline) and fetal/neonatal risks (macrosomia greater than 4000g, shoulder dystocia with brachial plexus injury, neonatal hypoglycemia, and RDS). Panel D: Management pyramid with medical nutrition therapy at the base, exercise at the next level, and pharmacotherapy at the top (insulin preferred, metformin alternative), with glucose targets table, growth ultrasound and NST surveillance, and delivery timing by GDM type.</image>

Section 6: Preterm Labor and Delivery

Preterm birth, defined as delivery before 37 weeks' gestation, complicates approximately 10% of pregnancies in the United States and is the leading cause of neonatal morbidity and mortality. Severity correlates inversely with gestational age at delivery.

Classification by gestational age guides prognosis and management intensity. Extremely preterm (<28 weeks) and very preterm (28-32 weeks) deliveries carry the highest risk of mortality and long-term complications including chronic lung disease, intraventricular hemorrhage, necrotizing enterocolitis, and neurodevelopmental impairment. Moderate to late preterm (32-37 weeks) outcomes are generally favorable but still associated with increased respiratory morbidity.

Risk factors for preterm birth include prior preterm birth (the single strongest predictor), short cervical length (<25 mm in mid-trimester), multiple gestation, uterine abnormalities (fibroids, müllerian anomalies), infection (urinary tract infection, bacterial vaginosis, chorioamnionitis), and social factors (smoking, low socioeconomic status, African American race).

Clinical presentation includes regular uterine contractions with cervical change (dilation and/or effacement). Patients may report pelvic pressure, low back pain, increased vaginal discharge, or bloody show. The challenge lies in distinguishing true preterm labor from preterm contractions without cervical change.

Diagnostic evaluation includes cervical examination for dilation and effacement. Fetal fibronectin (fFN), a glycoprotein that normally binds the fetal membranes to the decidua, is tested from cervicovaginal secretions; a negative fFN test (<50 ng/mL) has a high negative predictive value, indicating <1% probability of delivery within two weeks. Transvaginal ultrasound measurement of cervical length refines risk assessment: length ≥30 mm indicates low risk, while <25 mm significantly increases preterm birth probability.

Management goals include prolonging pregnancy to maximize fetal maturity while minimizing maternal risk. Tocolytic therapy does not prevent preterm birth but may delay delivery for 48 hours to allow corticosteroid administration and maternal transport to a higher-level facility. First-line tocolytics include calcium channel blockers (nifedipine) and indomethacin (a prostaglandin synthetase inhibitor, limited to <32 weeks due to fetal ductus arteriosus constriction risk). Magnesium sulfate and beta-agonists (terbutaline) are alternatives.

Antenatal corticosteroids are the most important intervention for improving neonatal outcomes. A course of betamethasone (two doses of 12 mg IM, 24 hours apart) or dexamethasone (four doses of 6 mg IM, 12 hours apart) accelerates fetal lung maturation, reducing respiratory distress syndrome, intraventricular hemorrhage, and neonatal death. Steroids are indicated for women at risk of preterm delivery between 24 and 34 weeks; a rescue course may be considered if the initial course was given more than 14 days prior.

Magnesium sulfate for neuroprotection, administered when delivery is anticipated before 32 weeks, reduces the risk of cerebral palsy.

<image>Panel A: Gestational age classification with outcomes showing extremely preterm (less than 28 weeks, high morbidity/mortality), very preterm (28-32 weeks, moderate risk), and late preterm (32-37 weeks, lower risk). Panel B: Diagnostic workup including cervical exam for dilation and effacement, fFN swab with negative result indicating less than 1% delivery in 2 weeks, and transvaginal ultrasound cervical length measurement with risk stratification (less than 25mm high risk, greater than 30mm low risk). Panel C: Tocolysis agents including nifedipine (first-line), indomethacin (less than 32 weeks with ductus warning), magnesium sulfate, and terbutaline, with central concept of delaying delivery to allow steroids and improve outcomes. Panel D: Antenatal corticosteroids showing betamethasone/dexamethasone dosing with optimal effect at 48 hours reducing RDS, IVH, and mortality, plus magnesium sulfate for neuroprotection before 32 weeks reducing cerebral palsy risk.</image>

Section 7: Premature Rupture of Membranes

Premature rupture of membranes (PROM) refers to rupture of the amniotic membranes before the onset of labor. When occurring before 37 weeks' gestation, it is termed preterm PROM (PPROM). PPROM complicates 3% of pregnancies and accounts for one-third of preterm births.

Diagnosis begins with history; patients typically report a sudden gush of fluid or continuous leakage from the vagina. A sterile speculum examination is performed, avoiding digital cervical examination, which increases infection risk without improving diagnostic accuracy in PPROM.

Three classic examination findings confirm membrane rupture. Pooling: visualization of amniotic fluid in the posterior vaginal fornix or leaking from the cervical os. Nitrazine testing: amniotic fluid (pH 7.0-7.5) turns nitrazine paper blue, while normal vaginal pH (4.5-5.5) does not; false positives occur with blood, semen, bacterial vaginosis, and alkaline antiseptics. Ferning: air-dried amniotic fluid on a glass slide demonstrates a fern-like crystallization pattern under microscopy. When clinical findings are equivocal, laboratory tests detecting placental proteins in vaginal secretions (AmniSure for PAMG-1, ROM Plus for IGFBP-1 and AFP) have high sensitivity and specificity.

Management of term PROM (≥37 weeks) involves delivery, as expectant management increases infection risk without improving outcomes. Labor induction, typically with oxytocin, is the preferred approach. If the patient is GBS-positive or status is unknown with risk factors, intrapartum antibiotic prophylaxis is administered.

Management of PPROM is more complex, balancing infection and compression risks against prematurity. At less than 34 weeks, expectant management prolongs pregnancy. This includes hospitalization, latency antibiotics (a 7-day course of ampicillin and azithromycin, or erythromycin, which extends the interval to delivery and reduces neonatal infection), antenatal corticosteroids, monitoring for infection (maternal temperature, fetal heart rate, uterine tenderness, laboratory markers), and serial assessment of amniotic fluid volume. Delivery is indicated for chorioamnionitis, non-reassuring fetal status, cord prolapse, significant vaginal bleeding, or reaching 34 weeks' gestation.

Between 34 and 37 weeks, management is individualized. Many experts recommend delivery at 34 weeks given improved neonatal outcomes and the diminishing benefit of expectant management. At ≥37 weeks, delivery proceeds promptly.

Complications of PPROM include chorioamnionitis (ascending infection causing maternal fever, fetal tachycardia, uterine tenderness), umbilical cord prolapse (emergency delivery required), placental abruption, and complications of prematurity. Early PPROM (<24 weeks) carries particular risk of pulmonary hypoplasia from prolonged oligohydramnios, limb deformities from compression, and extremely high mortality.

<image>Panel A: Diagnostic approach including patient history (gush of fluid), sterile speculum exam (avoiding digital exam), and three confirmation tests: pooling (fluid in vagina), nitrazine (pH paper turning blue), and ferning (microscope crystalline pattern), plus rapid tests (AmniSure/ROM Plus). Panel B: Management algorithm by gestational age showing less than 34 weeks with expectant management (hospitalization, ampicillin plus azithromycin, corticosteroids, monitoring), 34-37 weeks with individualized decision, and 37+ weeks with delivery by induction. Panel C: Latency antibiotic regimen showing days 1-7 course with outcomes of prolonged pregnancy and reduced infection rates. Panel D: Complications including chorioamnionitis (infected uterus with fever), cord prolapse (cord presenting at cervix), and oligohydramnios with pulmonary hypoplasia risk from early PPROM.</image>

Section 8: Placental Abnormalities

Placental abnormalities can cause life-threatening hemorrhage and represent critical obstetric emergencies. Understanding the distinct presentations of placenta previa, placental abruption, and vasa previa is essential.

Placenta previa occurs when the placenta implants over or near the internal cervical os. Classification includes complete previa (placenta completely covers the os), partial previa (placenta partially covers the os), marginal previa (placental edge reaches the os), and low-lying placenta (edge within 2 cm of the os). Early pregnancy ultrasounds frequently show low-lying placentas; most "migrate" away from the os as the lower uterine segment develops. Persistent previa occurs in approximately 0.5% of pregnancies at term. Risk factors include prior cesarean delivery, prior uterine surgery, multiparity, advanced maternal age, and multiple gestation.

The hallmark presentation is painless, bright red vaginal bleeding, typically in the late second or third trimester. The first bleeding episode ("sentinel bleed") may be minor, but subsequent episodes are often more severe. Digital cervical examination is absolutely contraindicated when previa is suspected, as it may provoke catastrophic hemorrhage. Diagnosis is made by transvaginal ultrasound, which accurately localizes the placenta. Management depends on gestational age and bleeding severity. Stable patients with preterm gestations are managed expectantly with pelvic rest, hospitalization for significant bleeding episodes, and serial ultrasounds. Delivery by cesarean section is planned at 36-37 weeks for uncomplicated cases, earlier if necessitated by hemorrhage.

Placental abruption is premature separation of the normally implanted placenta before delivery. It complicates 1% of pregnancies and accounts for 10% of perinatal mortality. Risk factors include chronic hypertension, preeclampsia, trauma (including motor vehicle accidents and domestic violence), cocaine use, smoking, prior abruption, and polyhydramnios with rapid decompression.

The classic presentation is painful vaginal bleeding with uterine tenderness, hypertonicity, and increased frequency of contractions. However, 20% of abruptions are concealed (blood trapped behind the placenta), presenting with pain and uterine findings but no vaginal bleeding. Severe abruption may cause disseminated intravascular coagulation. Fetal distress is common, ranging from abnormal heart rate patterns to death. Diagnosis is primarily clinical, as ultrasound sensitivity is only 50-80%; a negative ultrasound does not exclude abruption. Management depends on severity: mild abruption remote from term may allow expectant management with close monitoring, while significant abruption mandates delivery (vaginal if maternal and fetal status permit, cesarean for fetal distress or severe hemorrhage).

Vasa previa involves fetal vessels traversing the membranes over the internal cervical os, unprotected by placental tissue or umbilical cord. It occurs with velamentous cord insertion (cord inserts into membranes rather than placenta) and succenturiate placental lobes (accessory lobes with connecting vessels). The danger is vessel rupture when membranes rupture, causing rapid fetal exsanguination. Diagnosis by antenatal color Doppler ultrasound allows planned cesarean delivery before membrane rupture.

<image>Panel A: Placenta previa showing sagittal uterine diagram with complete previa covering internal os, painless bright red bleeding presentation, "NO digital exam" warning, transvaginal ultrasound with placenta over cervix, and management leading to cesarean delivery. Panel B: Placental abruption showing separated placenta with retroplacental clot, painful bleeding with uterine tenderness and contractions, risk factors (hypertension, cocaine, trauma), concealed versus revealed hemorrhage comparison, and fetal heart rate distress pattern. Panel C: Vasa previa showing velamentous cord insertion with vessels crossing the os, color Doppler ultrasound, fetal exsanguination danger if membranes rupture, and management with planned cesarean before labor. Panel D: Comparison table distinguishing previa (painless bleeding), abruption (painful bleeding), and vasa previa (fetal bleeding risk) with key diagnostic and management features for each.</image>

Section 9: Placenta Accreta Spectrum and Rh Incompatibility

Placenta accreta spectrum (PAS) disorders involve abnormal placental adherence to or invasion of the uterine wall due to defective decidualization. Three grades exist based on depth of invasion. Placenta accreta: villi attach directly to myometrium without intervening decidua. Placenta increta: villi invade into the myometrium. Placenta percreta: villi penetrate through the myometrium to the serosa or adjacent organs (bladder).

The dramatic increase in PAS disorders parallels rising cesarean delivery rates. Prior cesarean is the strongest risk factor; risk increases with each subsequent cesarean, reaching 6% with placenta previa and three prior cesareans. Other risk factors include prior uterine surgery, advanced maternal age, multiparity, and in vitro fertilization.

Prenatal diagnosis by ultrasound and MRI allows planned delivery at a tertiary center with multidisciplinary resources. Ultrasound findings suggestive of PAS include loss of the normal hypoechoic retroplacental clear zone, myometrial thinning, placental lacunae (irregular vascular spaces giving a "Swiss cheese" appearance), and abnormal color Doppler flow.

Management requires careful planning. Delivery by cesarean hysterectomy (leaving the placenta in situ, as attempted removal causes massive hemorrhage, followed by hysterectomy) is the standard approach for most cases. Timing is typically 34-36 weeks, after corticosteroids, balancing prematurity risk against the danger of spontaneous labor or bleeding. Blood products should be readily available, and interventional radiology for uterine artery balloon occlusion may be employed.

Rh incompatibility arises when an Rh-negative mother carries an Rh-positive fetus. Fetomaternal hemorrhage (fetal blood entering maternal circulation) exposes the mother to the D antigen, potentially triggering maternal anti-D IgG antibody production. In subsequent Rh-positive pregnancies, these IgG antibodies cross the placenta, attack fetal red blood cells, and cause hemolytic disease of the fetus and newborn (HDFN), ranging from mild anemia to hydrops fetalis and death.

Prevention with Rh immune globulin (RhoGAM) has made severe HDFN rare. RhoGAM (anti-D IgG) binds and eliminates fetal Rh-positive cells from maternal circulation before they can stimulate an immune response. The standard dose (300 μg IM) covers approximately 30 mL of fetal blood. RhoGAM is administered to unsensitized Rh-negative women at 28 weeks' gestation (when fetomaternal hemorrhage risk increases), within 72 hours postpartum if the newborn is Rh-positive, and after any sensitizing event (miscarriage, ectopic pregnancy, amniocentesis, trauma, vaginal bleeding, external cephalic version).

For Rh-negative women who are already sensitized (anti-D antibodies present), RhoGAM is not beneficial. These pregnancies require close monitoring with serial antibody titers and, when titers rise, middle cerebral artery (MCA) Doppler assessment. Elevated MCA peak systolic velocity (>1.5 multiples of the median) indicates fetal anemia. Severely affected fetuses may require intrauterine transfusion.

<image>Panel A: Placenta accreta spectrum with cross-sectional uterine diagrams showing three grades: accreta (villi touching myometrium), increta (villi invading into myometrium), and percreta (villi through myometrium to bladder), with risk factor bar graph showing increasing risk with prior cesareans and concurrent previa. Panel B: PAS diagnosis and management showing ultrasound with lacunae and abnormal Doppler findings, and cesarean hysterectomy with surgical team and blood product preparation. Panel C: Rh incompatibility pathophysiology showing Rh-negative mother, Rh-positive fetus, fetomaternal hemorrhage triggering maternal anti-D production, second pregnancy with antibodies crossing placenta and attacking fetal RBCs, and hydrops fetalis with edema, ascites, and pericardial effusion. Panel D: Rh incompatibility prevention and monitoring showing RhoGAM timeline at 28 weeks and postpartum plus after sensitizing events, antibody titer graph, MCA Doppler waveform with PSV greater than 1.5 MoM indicating anemia, and intrauterine transfusion for severe cases.</image>

Section 10: Multiple Gestation and Other Pregnancy Complications

Multiple gestation occurs in approximately 3% of pregnancies, increased by assisted reproductive technologies. Understanding chorionicity and amnionicity is critical, as monochorionic pregnancies carry substantially higher risk.

Dizygotic (fraternal) twins result from fertilization of two separate ova by two sperm. They are always dichorionic (separate placentas) and diamniotic (separate amniotic sacs). Monozygotic (identical) twins result from division of a single fertilized ovum; their chorionicity and amnionicity depend on timing of division. Division before day 4 produces dichorionic/diamniotic twins. Division between days 4-8 produces monochorionic/diamniotic twins (shared placenta, separate sacs). Division between days 8-13 produces monochorionic/monoamniotic twins (shared placenta and sac). Division after day 13 produces conjoined twins.

Ultrasound determination of chorionicity, ideally in the first trimester, is essential. Dichorionic twins show a thick dividing membrane with a "twin peak" or "lambda" sign (placental tissue extending between membranes at the base). Monochorionic/diamniotic twins show a thin membrane with a "T-sign" (membranes meeting placenta at right angle).

All multiple gestations carry increased risk of preterm delivery, preeclampsia, gestational diabetes, and intrauterine growth restriction. Monochorionic twins face additional complications from shared placental circulation. Twin-twin transfusion syndrome (TTTS) occurs when unbalanced blood flow through placental vascular anastomoses causes one twin (donor) to become anemic, growth-restricted, and oligohydramniotic while the other twin (recipient) becomes polycythemic, volume-overloaded, and polyhydramniotic. TTTS is staged by severity (Quintero stages I-V) and treated by fetoscopic laser ablation of the anastomosing vessels. Monoamniotic twins face cord entanglement risk, necessitating intensive surveillance and early delivery.

Other pregnancy complications merit brief mention. Hyperemesis gravidarum is severe nausea and vomiting causing >5% weight loss, ketonuria, and electrolyte disturbances, requiring IV hydration, antiemetics, and thiamine supplementation; molar pregnancy must be excluded. Intrahepatic cholestasis of pregnancy presents with pruritus (especially palms and soles) without primary rash, elevated serum bile acids, and increased stillbirth risk; ursodeoxycholic acid is the treatment, with delivery at 36-37 weeks. Acute fatty liver of pregnancy is a rare but life-threatening condition causing liver failure with coagulopathy, hypoglycemia, and encephalopathy; emergency delivery is required. Peripartum cardiomyopathy presents as heart failure (LVEF <45%) occurring from the last month of pregnancy through five months postpartum; treatment follows standard heart failure management with delivery timing based on maternal status.

<image>Panel A: Twin types showing dizygotic pathway (two eggs, two sperm, always dichorionic/diamniotic) and monozygotic pathway with timing-dependent chorionicity/amnionicity (day 0-14 timeline), plus ultrasound images of lambda sign (DC twins) versus T-sign (MC twins). Panel B: Twin-twin transfusion syndrome showing donor twin (small, oligohydramnios) and recipient twin (large, polyhydramnios) with connecting vessels, Quintero staging summary, and fetoscopic laser ablation treatment, plus monoamniotic twins with cord entanglement. Panel C: Hyperemesis gravidarum (emesis, IV fluids, thiamine supplementation) and intrahepatic cholestasis of pregnancy (pruritus of palms/soles, elevated bile acids, delivery at 36-37 weeks). Panel D: Acute fatty liver of pregnancy (liver failure signs, emergency delivery) and peripartum cardiomyopathy (dilated heart on echo with LVEF less than 45%, heart failure symptoms and standard management).</image>

Summary

Routine prenatal care follows a structured schedule of increasing visit frequency (monthly through 28 weeks, biweekly 28-36 weeks, weekly 36-40 weeks) with standardized assessments including blood pressure, weight, fundal height, and fetal heart tones. Initial laboratory evaluation screens for blood type, antibodies, anemia, infections, and rubella immunity.

Prenatal screening distinguishes risk assessment from diagnosis. First-trimester combined screening, second-trimester quad screen, and cell-free DNA all screen for aneuploidy, with positive results requiring diagnostic confirmation via CVS or amniocentesis.

Hypertensive disorders are classified as chronic hypertension, gestational hypertension, preeclampsia, and eclampsia. Preeclampsia is hypertension after 20 weeks plus proteinuria or end-organ dysfunction. Delivery is the only cure; magnesium sulfate prevents seizures; antihypertensives treat severe hypertension.

Gestational diabetes screening at 24-28 weeks uses either one-step (75g OGTT) or two-step (50g challenge, then 100g OGTT) approaches. Management includes medical nutrition therapy, exercise, and pharmacotherapy (insulin preferred) with glucose targets: fasting <95, 1-hour postprandial <140.

Preterm labor is managed with tocolysis to delay delivery 48 hours, antenatal corticosteroids for lung maturity (24-34 weeks), and magnesium sulfate for neuroprotection (<32 weeks). PPROM management balances infection risk against prematurity, with latency antibiotics prolonging pregnancy.

Placenta previa presents with painless vaginal bleeding; digital exam is contraindicated; cesarean delivery is required. Placental abruption presents with painful bleeding and uterine tenderness; management depends on severity. Placenta accreta spectrum requires planned cesarean hysterectomy.

Rh incompatibility is prevented by RhoGAM administration at 28 weeks and postpartum. Sensitized pregnancies require MCA Doppler surveillance and possible intrauterine transfusion.

Multiple gestation chorionicity determines risk; monochorionic twins face TTTS and cord entanglement risks.

Key Terms

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