3.2 Ectopic Pregnancy, Placenta Previa, Accreta Spectrum (PAS), Abruption & Vasa Previa

Placenta Previa, Accreta Spectrum (PAS), Abruption & Vasa Previa

Third-trimester vaginal bleeding is an acute obstetric emergency affecting 3% to 5% of all pregnancies. Rapid differentiation among placenta previa, placenta accreta spectrum (PAS), placental abruption, and vasa previa is essential to prevent catastrophic maternal hemorrhagic shock and rapid fetal demise.

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|                   CRITICAL CARDINAL RULE OF THIRD-TRIMESTER BLEEDING                  |
|                                                                                       |
|   NEVER PERFORM A DIGITAL VAGINAL EXAMINATION ON A PATIENT WITH THIRD-TRIMESTER       |
|   VAGINAL BLEEDING UNTIL PLACENTAL LOCATION HAS BEEN DEFINITIVELY CONFIRMED           |
|   BY ULTRASOUND TO RULE OUT PLACENTA PREVIA AND VASA PREVIA.                          |
|                                                                                       |
|   Digital exam in previa/vasa previa can directly tear placental sinuses or fetal     |
|   vessels, triggering immediate, fatal maternal or fetal exsanguination.              |
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1. Placenta Previa & Low-Lying Placenta

Placenta previa occurs when the placenta implants in the lower uterine segment, directly overlying or abutting the internal cervical os.

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|                               PLACENTA PREVIA SPECTRUM                                |
|                                                                                       |
|   [Placenta Previa]                                                                   |
|   - The internal cervical os is completely covered by the placenta                    |
|   - Transvaginal US measurement: Overlaps internal os (distance = 0 mm)               |
|   - Mode of delivery: Mandatory Cesarean Delivery                                     |
|                                                                                       |
|   [Low-Lying Placenta]                                                                |
|   - Placental edge is located within 20 mm (2.0 cm) of the internal cervical os      |
|   - Does not directly cover the internal os                                           |
|   - Mode of delivery: Trial of labor feasible if distance is 10–20 mm and no bleeding|
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Clinical Presentation & Pathophysiology:

• Presentation: Sudden onset of painless, bright red vaginal bleeding in the late second or third trimester. The bleeding is maternal in origin, caused by mechanical shearing of the inelastic placenta away from the thinning, elongating lower uterine segment and dilating cervix.
• Physical Exam Findings: The uterus is soft, non-tender, and relaxed with normal resting tone. Fetal heart rate is typically reassuring unless maternal hypovolemic shock ensues.
• Risk Factors: Prior cesarean delivery (strongest predictor), advanced maternal age (>35 years), multiparity, prior uterine curettage or myomectomy, cigarette smoking, living at high altitudes, and multifetal gestation.
• Diagnostic Standard: Transvaginal Ultrasonography (TVS) is the gold standard (safe, accurate, with 99% sensitivity; transabdominal US has a 25% false-positive rate due to bladder overfilling and myometrial contractions).
• Management Guidelines (ACOG/SMFM):
  • Pelvic Rest: Strict prohibition of sexual intercourse, tampon use, and digital cervical exams.
  • Active Bleeding Episode: Admit to labor & delivery, large-bore IV access (two 16-gauge or 18-gauge lines), type and crossmatch 2–4 units PRBCs, continuous fetal and uterine monitoring, administer antenatal corticosteroids (betamethasone) if <37 weeks, and Rh immune globulin (RhoGAM) if Rh-negative.
  • Delivery Timing: Scheduled cesarean delivery at 36 0/7 to 37 6/7 weeks of gestation for uncomplicated placenta previa. If recurrent heavy bleeding, hemodynamic instability, or non-reassuring fetal status occurs, immediate emergent cesarean is indicated regardless of gestational age.

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2. Placenta Accreta Spectrum (PAS)

Placenta Accreta Spectrum (PAS) refers to the range of pathologic placental adherence where trophoblast tissue attaches directly to or invades into the myometrium due to a total or partial defect in the decidua basalis (Nitabuch's layer).

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|                       PLACENTA ACCRETA SPECTRUM (PAS) DEPTH                           |
|                                                                                       |
|   [1. Placenta Accreta Vera (~75–80% of PAS)]                                         |
|   - Chorionic villi attach directly to the myometrium surface without invasion        |
|                                                                                       |
|   [2. Placenta Increta (~15% of PAS)]                                                 |
|   - Chorionic villi invade deeply INTO the myometrial muscle wall                     |
|                                                                                       |
|   [3. Placenta Percreta (~5% of PAS)]                                                 |
|   - Chorionic villi invade THROUGH the entire myometrium, breach the uterine serosa,  |
|     and frequently invade adjacent pelvic organs (e.g., posterior bladder wall)       |
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Epidemiologic Risk Multiplier:

The synergistic combination of prior cesarean delivery and a concurrent placenta previa is the single greatest risk factor for PAS:

Antenatal Imaging & Diagnostic Findings:

• Ultrasound & Color Doppler Markers: Loss of the normal retroplacental hypoechoic clear zone, multiple large irregular placental vascular lacunae (creating a "Swiss cheese" or "moth-eaten" appearance), turbulent high-velocity lacunar flow on Doppler, myometrial thinning to <1 mm, and bladder line disruption with bridging vessels traversing into the bladder wall (percreta).
• Magnetic Resonance Imaging (MRI): Highly valuable for posterior placenta accreta or assessing the precise depth of parametrial and bladder wall invasion in suspected placenta percreta (demonstrating dark T2 intraplacental bands, focal uterine bulging, and bladder tenting).

Modern Clinical Management of PAS:

1. Level of Care & Multidisciplinary Team: Delivery must occur at a Level III or Level IV Maternal Care Facility by a dedicated multidisciplinary PAS team: Maternal-Fetal Medicine, Gynecologic Oncology, Obstetric Anesthesiology, Trauma/Vascular Surgery, Interventional Radiology, Blood Bank, and Neonatology.
2. Planned Delivery Timing: Scheduled cesarean delivery at 34 0/7 to 35 6/7 weeks of gestation, balancing fetal lung maturity against the escalating risk of unscheduled emergency hemorrhage from spontaneous labor.
3. Surgical Protocol (Gold Standard):
   • Vertical midline abdominal incision for wide pelvic exposure.
   • Ultrasound-guided uterine mapping: Direct intraoperative ultrasound to map the upper placental margin.
   • Classical or Fundal Hysterotomy: The uterine incision is made high in the uterine fundus, completely avoiding the anterior placental bed.
   • Infant Delivery & Umbilical Cord Ligation: Deliver the infant, clamp and cut the cord at the insertion site, and close the hysterotomy.
   • NO ATTEMPT AT PLACENTAL REMOVAL: Never attempt to peel, manually extract, or dissect the placenta. Manual disruption of the accreta placental bed triggers catastrophic, torrential hemorrhage (>3,000–5,000 mL within minutes).
   • Immediate Planned Cesarean Hysterectomy: Proceed directly with the placenta left entirely in situ.

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3. Placental Abruption (Abruptio Placentae)

Placental abruption is the premature detachment of a normally implanted placenta from the myometrium prior to the delivery of the fetus, occurring in approximately 1% of pregnancies.

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|                        PLACENTAL ABRUPTION PATHOPHYSIOLOGY                            |
|                                                                                       |
|   [Decidual Spiral Artery Rupture]                                                    |
|                 |                                                                     |
|                 v                                                                     |
|   [Retroplacental Hematoma Formation]                                                 |
|                 |                                                                     |
|                 +--------------------------------+                                    |
|                 |                                |                                    |
|                 v (80% of cases)                 v (20% of cases)                     |
|   [Revealed / External Bleeding]       [Concealed / Internal Bleeding]                |
|   - Blood tracks between membranes     - Blood trapped behind placenta/membranes      |
|     and exits through cervix           - Fundal height increases rapidly              |
|   - Visible dark red hemorrhage        - Severe abdominal pain, board-like uterus     |
|                 |                                |                                    |
|                 +--------------------------------+                                    |
|                 |                                                                     |
|                 v                                                                     |
|   [Massive Decidual Tissue Factor (TF) Release into Maternal Circulation]             |
|                 |                                                                     |
|                 v                                                                     |
|   [Fulminant Consumptive Coagulopathy / Obstetric DIC & Fetal Hypoxia]                |
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Clinical Presentation & Diagnosis:

• The Classic Abruption Triad:
  1. Painful, dark red ('prune juice') vaginal bleeding (present in 80%; absent in 20% concealed abruption).
  2. Severe, continuous abdominal and uterine back pain.
  3. Uterine hypertonicity, baseline tachysystole (>5 contractions/10 min), and elevated resting uterine tone ('board-like' or 'woody' uterus upon palpation).
• Fetal Impact: Decreased placental surface area for gas exchange triggers fetal distress: repetitive late decelerations, loss of variability, profound prolonged bradycardia, or intrauterine fetal demise (IUFD).
• Ultrasound Limitations: Ultrasound has a low sensitivity (25% to 50%) for detecting acute placental abruption because acute retroplacental hematomas are isoechoic with the placenta. A negative ultrasound NEVER rules out placental abruption. Abruption remains a clinical diagnosis.
• Couvelaire Uterus (Uteroplacental Apoplexy): Widespread extravasation of blood into the myometrium and beneath the uterine serosa, giving the uterus a mottled, dark purple or ecchymotic appearance during laparotomy. It impairs myometrial contractility, predisposing to profound postpartum atony.
• Consumptive Coagulopathy: Placental abruption is the most common obstetric cause of Disseminated Intravascular Coagulation (DIC), triggered by the massive systemic release of decidual tissue factor into maternal veins.

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4. Vasa Previa

Vasa previa is an acute, catastrophic condition in which unprotected fetal blood vessels course through the amniotic membranes across or within 2 cm of the internal cervical os, unsupported by the placenta or Wharton's jelly.

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|                                   VASA PREVIA PROFILE                                 |
|                                                                                       |
|   [Anatomic Varieties]                                                                |
|   - Type I: Velamentous cord insertion with membranous vessels traversing the os      |
|   - Type II: Membranous vessels connecting a succenturiate lobe or bilobed placenta   |
|                                                                                       |
|   [The Catastrophic Cascade]                                                          |
|   - Membrane Rupture (SROM or AROM) directly tears the traversing fetal vessels       |
|   - Rapid fetal exsanguination (Total fetal blood volume is only ~80–100 mL/kg!)      |
|                                                                                       |
|   [Clinical Triad of Acute Rupture]                                                   |
|   1. Spontaneous or artificial rupture of membranes (SROM/AROM)                       |
|   2. Painless, bright red vaginal bleeding occurring simultaneously                   |
|   3. Immediate fetal distress: Sinusoidal FHR pattern or severe fetal bradycardia     |
|                                                                                       |
|   [Emergency Management]                                                              |
|   - STAT Emergent Cesarean Delivery within minutes (do NOT await lab testing)         |
|   - Immediate Neonatal Resuscitation + Uncrossed O-Negative Blood Transfusion         |
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Diagnostic & Clinical Pearls for Vasa Previa:

• Fetal Hemodynamic Vulnerability: A term fetus has a total blood volume of only ~250 to 300 mL. Loss of even 50 to 100 mL of blood represents 20% to 40% of the entire circulating fetal volume, producing immediate hemorrhagic shock, irreversible cerebral ischemia, and death within minutes.
• Sinusoidal FHR Pattern: The hallmark cardiotocographic finding of acute fetal anemia is a true sinusoidal pattern (smooth, undulating sine-wave baseline with a cycle frequency of 3–5 cycles per minute and amplitude of 5–15 bpm lasting >20 minutes) or sudden catastrophic sustained bradycardia.
• Bedside Diagnostic Tests for Fetal Blood:
  • Apt Test / Ogita Test: Differentiates fetal hemoglobin (HbF, which is alkali-resistant) from adult maternal hemoglobin (HbA, which is alkali-sensitive). Adding 1% sodium hydroxide (NaOH) turns maternal blood yellow-brown, while fetal blood remains pink.
  • Kleihauer-Betke Test: Acid elution test quantifying fetal red blood cells in maternal blood, useful for dosing Rh immune globulin, but too slow for acute intrapartum emergency decision-making.
  • Clinical Reality: In acute intrapartum vasa previa rupture, do not waste time performing bedside tests. Immediate emergent delivery is required to save the infant.
• Antenatal Screening & Management: Color and pulsed Doppler transvaginal ultrasound detects vasa previa with >95% accuracy. When diagnosed prenatally: planned hospitalization at 30–34 weeks, administration of corticosteroids, and scheduled cesarean delivery at 34 0/7 to 35 6/7 weeks (prior to the onset of labor or membrane rupture).

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5. Third-Trimester Bleeding: Comparative Clinical Matrix

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6. Ectopic Pregnancy: The First-Trimester Hemorrhagic Emergency

The NCC outline lists ectopic pregnancy first under Hemorrhage. It belongs with the placental disorders above because all of them are failures of implantation site, but it is the one that presents in the first trimester, often to an emergency department rather than to labor and delivery, and ruptured ectopic pregnancy remains the leading cause of first-trimester maternal death. Over 90% of ectopic implantations are tubal, most commonly in the ampulla.

Recognition: Why It Is Missed

The classic triad — amenorrhea, unilateral pelvic pain, and vaginal bleeding — is present in a minority of patients. The lethal presentation is hemorrhagic shock with a deceptively benign external examination, because the blood is intraperitoneal:

• Minimal or absent vaginal bleeding. External blood loss badly underestimates internal loss; the cervix is typically closed.
• Referred shoulder-tip pain (Kehr sign) from diaphragmatic irritation by hemoperitoneum, and pain with movement or defecation from pelvic blood.
• Rebound tenderness, guarding, or a rigid abdomen, cervical motion tenderness, and a fullness in the cul-de-sac.
• Syncope or near-syncope, tachycardia, and a narrowed pulse pressure — the same compensated-shock physiology taught in Section 1.3.

Operational rule: a positive pregnancy test plus hypotension or abdominal pain in a patient whose pregnancy has not been localized is a ruptured ectopic pregnancy until proven otherwise. Risk factors (prior ectopic, tubal surgery or damage, pelvic inflammatory disease, in vitro fertilization, intrauterine device in place, smoking) raise suspicion but their absence never lowers it.

Diagnosis: Transvaginal Ultrasound Plus hCG

Diagnosis rests on transvaginal ultrasonography interpreted alongside serum hCG. ACOG cautions that if the hCG discriminatory level — the value above which a normal intrauterine pregnancy should be visible — is used at all, it should be set conservatively high, as high as 3,500 mIU/mL, to avoid misdiagnosing and inadvertently interrupting a desired viable intrauterine pregnancy. Multiple gestations may exceed traditional thresholds without a visible sac. A pregnancy of unknown location is followed with serial hCG, never with a single value.

Medical Management: Methotrexate

Methotrexate is an option only for the hemodynamically stable patient who can reliably return for follow-up.

Absolute contraindications include a ruptured ectopic pregnancy, hemodynamic instability, inability to participate in follow-up, breastfeeding, immunodeficiency, moderate-to-severe anemia, leukopenia or thrombocytopenia, clinically important hepatic or renal dysfunction, active peptic ulcer disease, active pulmonary disease, methotrexate sensitivity, and a coexisting intrauterine pregnancy. Relative contraindications include embryonic cardiac activity on transvaginal ultrasound, a high initial hCG, an ectopic mass larger than 4 cm, and refusal of blood transfusion. An hCG above roughly 5,000 mIU/mL and a rise of more than 50% in 48 hours both predict methotrexate failure. Counsel patients to avoid nonsteroidal anti-inflammatory drugs, folic acid supplements, alcohol, and sun exposure during treatment.

Surgical Management and the Unstable Patient

• Unstable or ruptured: activate the massive transfusion protocol, resuscitate with balanced blood products, and move to the operating room. Do not delay definitive surgery for confirmatory imaging or for a methotrexate discussion — laparotomy is appropriate when instability precludes laparoscopy.
• Salpingectomy is generally the preferred operation. Salpingostomy is reserved for the patient wishing to preserve fertility when the contralateral tube is absent or damaged, and it mandates serial post-operative hCG surveillance for persistent trophoblastic tissue.
• Rh D-negative patients require anti-D immune globulin after an ectopic pregnancy.