10.3 Antepartum Haemorrhage: Placenta Praevia & Placental Abruption

Definition, Epidemiology & Initial Triage of Antepartum Haemorrhage

Antepartum haemorrhage (APH) is defined as bleeding from or into the genital tract occurring from the threshold of fetal viability—conventionally 20 to 24 weeks of gestation—until the completion of fetal delivery. Complicating approximately 3% to 5% of all pregnancies, APH represents an acute obstetric crisis associated with substantial maternal hypovolemic shock, operative delivery, disseminated intravascular coagulation, iatrogenic extreme prematurity, and intrauterine fetal demise.

The etiologies of APH are categorized into four distinct groups:

• Placental Site Bleeding (approx. 70%): Placental abruption (abruptio placentae, ~30% to 35%) and placenta praevia (~30% to 35%).
• Fetal Vascular Origin (< 1%): Ruptured vasa praevia.
• Uterine Myometrial Disruption (< 1%): Complete uterine rupture (primarily encountered in laboring gravidas with prior scarred uteri).
• Local / Incidental Lower Genital Tract Lesions (~20% to 25%): Severe cervicitis, cervical polyps, cervical ectropion, invasive cervical carcinoma, and trauma or vaginal tears.

The Emergency Triage & Resuscitation Bundle

Every gravida presenting with third-trimester vaginal bleeding must be managed according to standardized emergency trauma/resuscitation principles:

1. Primary Survey & Left Lateral Position: Immediately assess airway, breathing, and circulatory dynamics. Tilt the patient 15° to 30° into the left lateral decubitus position or manually displace the gravid uterus to the left to decompress the inferior vena cava and restore venous return.
2. Large-Bore Vascular Access: Place two large-bore intravenous cannulae (14 or 16-gauge) in antecubital veins. Infuse warmed crystalloids (0.9% normal saline or Hartmann's solution) under pressure.
3. Emergency Laboratory Diagnostic Workup: Draw immediate baseline bloods: Complete blood count (CBC) with platelet count, blood group and crossmatch for 4 to 6 units of packed red blood cells, coagulation profile (prothrombin time [PT/INR], activated partial thromboplastin time [aPTT], and quantitative fibrinogen), renal and liver biochemistry, and a Kleihauer-Betke test in RhD-negative gravidas.
4. Fetal & Uterine Monitoring: Initiate continuous electronic fetal monitoring (cardiotocography [CTG]) if the fetus is viable (>= 24 weeks). Palpate the abdomen to determine uterine tone, tenderness, contraction frequency, and fetal presentation.
5. Absolute Prohibition of Digital Vaginal Examination: A digital vaginal examination (PV) is strictly and absolutely contraindicated in any patient with antepartum hemorrhage until the placental location has been verified by ultrasound imaging. Blind digital examination can disrupt low-lying placental cotyledons, triggering catastrophic, uncontainable hemorrhage that can result in maternal and fetal exsanguination within minutes. A gentle sterile speculum examination is safe even when placenta praevia is suspected, and may identify a cervical or vaginal bleeding source. This differs from digital cervical examination, which must await exclusion of praevia.

Placenta Praevia: Pathogenesis, Spectrum & Management

Placenta praevia occurs when the placenta implants wholly or partially within the lower uterine segment, overlying or lying in close proximity to the internal cervical os. The lower uterine segment begins to develop, elongate, and thin out during the late second and third trimesters. Mechanical shearing forces between the expanding lower uterine segment and the non-elastic placental attachment tear low-pressure maternal decidual venous sinuses, leading to recurrent hemorrhage. Bleeding in placenta praevia is almost exclusively maternal in origin.

Classification & Predisposing Factors

Contemporary ultrasonographic classification stratifies placenta praevia based on transvaginal ultrasonography (TVS) measurements:

• Placenta Praevia: Placental tissue partially or completely covers the internal cervical os.
• Low-Lying Placenta: The placental edge lies within 20 mm (2 cm) of the internal cervical os, but does not cover it.

Major predisposing risk factors include:

• Prior Cesarean Delivery: A major risk factor, with risk increasing as the number of previous cesarean scars rises. RCOG cites an increase in placenta praevia from about 1% after one prior cesarean to about 2.8% after multiple prior cesareans.
• Prior Uterine Surgery: Uterine curettage, operative hysteroscopy, or myomectomy.
• Multiparity & Advanced Maternal Age: Maternal age > 35 years carries a threefold increased risk.
• Multiple Gestation: Expanded placental surface area.
• Cigarette Smoking: Placental hypertrophy secondary to carbon monoxide-induced tissue hypoxemia.

Clinical Presentation & Physical Hallmarks

The classic clinical presentation is sudden-onset, entirely painless, bright red vaginal bleeding, frequently awakening the patient from sleep. Key physical findings include:

• The uterus is completely soft, relaxed, and non-tender, with no hypertonus.
• Fetal heart sounds are typically normal and reassuring during initial bleeding episodes because maternal blood loss has not yet produced hemodynamic collapse.
• High, floating, unengaged fetal presenting part, or abnormal fetal lie (transverse, oblique, or breech) in over 30% of cases, because the placenta mechanically obstructs the pelvic inlet.

Placenta Accreta Spectrum (PAS)

Placenta accreta spectrum represents abnormal, morbid adherence of chorionic villi directly to or into the myometrium due to a localized defect in the decidua basalis (Nitabuch's layer), almost invariably occurring at the site of a previous cesarean hysterotomy scar. The spectrum includes:

• Placenta Accreta: Chorionic villi adhere directly to the myometrium without muscular invasion (75% to 80% of PAS cases).
• Placenta Increta: Chorionic villi invade deeply into the myometrium (15% of cases).
• Placenta Percreta: Chorionic villi penetrate completely through the full thickness of the myometrium, breaching the uterine serosa and frequently invading adjacent pelvic viscera, predominantly the bladder wall (5% of cases).

In women with a placenta praevia overlying an anterior lower segment cesarean scar, the risk of PAS is extraordinarily high: ~10% with 1 prior cesarean, ~40% with 2, and > 50% to 60% with 3 or more. Attempting manual removal of an accreta placenta during delivery produces massive, life-threatening hemorrhage. Management mandates planned multidisciplinary delivery at 34+0 to 35+6 weeks in a tertiary care center, performing a cesarean delivery with the infant delivered via a high fundal hysterotomy incision away from the placenta, followed by planned cesarean hysterectomy without disturbing the adherent placenta.

Management Protocol for Placenta Praevia

• Asymptomatic Antenatal Diagnosis: If a low-lying placenta is identified during the routine 18 to 20-week anatomy scan, > 90% will resolve by term due to "placental migration" (differential growth of the lower uterine segment away from the cervix). Follow-up transvaginal ultrasound is scheduled at 32 and 36 weeks.
• Symptomatic Bleeding Episodes: Requires immediate inpatient hospitalization, bed rest, two large-bore IVs, blood crossmatching, and administration of antenatal corticosteroids (betamethasone or dexamethasone) if between 24 and 36+6 weeks. RhD-negative gravidas receive 1,500 IU anti-D immunoglobulin.
• Definitive Delivery Timing: In stable, asymptomatic placenta praevia, planned elective cesarean section is performed at 36+0 to 37+6 weeks. If active, uncontrollable, torrential hemorrhage or maternal/fetal compromise supervenes, immediate emergency cesarean delivery is executed regardless of gestational age.

Placental Abruption: Concealed Hemorrhage, DIC & Couvelaire Uterus

Placental abruption (abruptio placentae) is the premature separation of a normally implanted placenta from the uterine decidua basalis prior to delivery of the infant. The initiating pathophysiological event is spontaneous or traumatic rupture of maternal decidual spiral arterioles. The escaping high-pressure arterial blood forms an expanding retroplacental hematoma that shears the decidual junction, stripping placental villi from the uterine wall and extinguishing maternal-fetal gas exchange.

Clinical Varieties: Revealed vs. Concealed

• Revealed (External) Abruption (80%): Blood dissects downward between the fetal membranes and the uterine wall, escaping through the cervical os as dark vaginal bleeding.
• Concealed (Internal) Abruption (20%): Blood remains entirely trapped behind the detached placenta and membranes. Because no external bleeding is observed, the clinical severity of the hemorrhage is frequently missed. The patient develops profound hypovolemic shock, severe abdominal pain, and fetal death out of all proportion to visible blood loss.

Etiological Risk Factors

• Maternal Hypertensive Disorders: Chronic hypertension, gestational hypertension, and pre-eclampsia account for almost 50% of severe abruptions.
• Blunt Abdominal Trauma: Motor vehicle collisions and domestic interpersonal violence (shearing forces tear the inelastic placenta from the pliable elastic uterus).
• Sudden Uterine Decompression: Rapid loss of amniotic fluid following rupture of membranes in polyhydramnios, or following delivery of the first infant in a twin gestation.
• Cocaine / Crack Cocaine & Tobacco Abuse: Intense transient vasoconstriction and microvascular decidual necrosis.
• Previous Abruption: Recurrence risk is 10% after one prior abruption, rising to 25% after two.

Clinical Presentation: The Classic Tetrad

The diagnostic hallmark of placental abruption is the sudden onset of:

1. Severe, Unremitting Abdominal or Lower Back Pain
2. Dark Vaginal Bleeding (absent in concealed abruption)
3. Uterine Hypertonus & Extreme Tenderness: The uterus feels hard, rigid, board-like ("woody"), with sustained baseline tone and inability to relax between high-frequency contractions.
4. Fetal Compromise or Intrauterine Fetal Demise (IUFD): Fetal bradycardia, severe late decelerations, or absent fetal heart tones.

Severe Systemic Complications

• Consumptive Disseminated Intravascular Coagulation (DIC): Extensive mechanical damage to the decidua and placenta releases massive quantities of tissue factor (thromboplastin) directly into the maternal circulation. This triggers widespread systemic thrombin generation, rapid microvascular fibrin deposition, and exhaustion of circulating platelets, prothrombin, and fibrinogen. Serum fibrinogen levels plummet rapidly. In pregnancy, normal plasma fibrinogen is elevated (4.0 to 6.0 g/L); a fibrinogen concentration < 2.0 g/L indicates severe, critical consumption, while levels < 1.5 g/L predict massive life-threatening hemorrhage.
• Couvelaire Uterus (Uteroplacental Apoplexy): Retroplacental blood under high pressure dissects into the interlacing muscle bundles of the myometrium and beneath the peritoneal serosa of the uterus. Upon laparotomy, the uterus exhibits a mottled, bruised, dark purple or bluish discoloration. Couvelaire uterus causes severe myometrial atony, dramatically escalating the risk of refractory postpartum hemorrhage.
• Acute Kidney Injury (AKI): Renal tubular and bilateral renal cortical necrosis driven by prolonged hypovolemic shock and microthrombosis.

Critical Ultrasound Rule: Ultrasonography has notoriously low diagnostic sensitivity for placental abruption (only 25% to 50%), because acute retroplacental hematomas have identical echogenicity to adjacent normal placental tissue. A normal ultrasound scan does NOT rule out placental abruption. The diagnosis is strictly clinical.

Management of Placental Abruption

Immediate stabilization with crystalloid and rapid blood component therapy (packed RBCs, fresh frozen plasma [FFP], cryoprecipitate if fibrinogen < 1.5 to 2.0 g/L, and platelets):

• Viable Fetus with Fetal Distress or Maternal Instability: Execute an immediate emergency Category 1 cesarean delivery with concurrent aggressive blood component resuscitation.
• Intrauterine Fetal Demise (IUFD): Fetal death suggests severe abruption and requires urgent assessment for hypovolemia and coagulopathy; it does not by itself quantify placental separation or establish DIC. If the mother is hemodynamically resuscitated and coagulopathy is actively corrected with blood products, vaginal delivery is the preferred route. Performing an emergency laparotomy in the presence of uncorrected DIC carries extreme operative mortality. Artificial rupture of membranes (amniotomy) is performed immediately to decompress the uterus, diminish thromboplastin extravasation, and stimulate labor, accompanied by titrated intravenous oxytocin infusion.

Vasa Praevia & Miscellaneous APH Etiologies

Vasa Praevia

Vasa praevia occurs when fetal blood vessels within the membranes run across the internal cervical os unprotected by the umbilical cord's Wharton's jelly or placental tissue. It is classically associated with velamentous cord insertion (umbilical cord inserts into the membranes rather than the placental mass) or a succenturiate (accessory) placental lobe connected by aberrant intramembranous vessels.

• Clinical Presentation: The pathognomonic presentation is painless, fresh vaginal bleeding occurring immediately upon rupture of membranes (spontaneous or artificial amniotomy), rapidly followed by profound fetal bradycardia, a sinusoidal heart rate pattern on CTG, and fetal death within minutes.
• Pathophysiology: The torn vessels are fetal; because a term fetus has a total blood volume of only ~250 to 300 mL, the loss of even 50 to 100 mL of fetal blood produces fatal hypovolemic exsanguination.
• Diagnostic Differentiation: The Apt test (alkali denaturation using 1% sodium hydroxide) distinguishes maternal adult hemoglobin (HbA, which denatures and turns yellow-brown) from fetal hemoglobin (HbF, which is alkali-resistant and remains bright pink). However, in acute active bleeding, there is no time for laboratory tests.
• Management: Acute intrapartum vasa praevia rupture requires immediate crash cesarean delivery within minutes. When detected antenatally on transvaginal color Doppler ultrasound, planned elective cesarean delivery is performed at 34 to 36 weeks following antenatal corticosteroids.

Uterine Rupture

Complete disruption of all uterine layers including the visceral peritoneum, occurring predominantly in women attempting a trial of labor after cesarean (TOLAC) or prior transmyometrial surgery. Manifests with sudden agonizing abdominal pain, cessation of uterine contractions, "loss of fetal station" (presenting part recedes on vaginal exam), palpable fetal parts in the maternal abdomen, profound maternal hypovolemia, and prolonged fetal bradycardia. Requires immediate emergency laparotomy, fetal delivery, and uterine repair or hysterectomy.

Comparative Differential Diagnosis of Antepartum Haemorrhage