Placental Pathology & Peripartum Hemorrhage
Where the placenta sits, how deep it digs, and why mothers bleed
Placenta accreta spectrum
The decidual defect. Normally the decidua basalis, with its fibrinoid Nitabuch layer, separates anchoring villi from the myometrium and provides the cleavage plane along which the placenta peels away after birth. Where decidua is deficient, usually at a prior cesarean scar or the site of other uterine surgery (myomectomy, curettage), villi attach directly to myometrium. Risk climbs steeply with each prior cesarean when a placenta previa overlies the scar; the classic patient is a multiparous woman with two or more cesareans and an anterior previa.
- Accreta: villi attach to the myometrial surface; the most common grade.
- Increta: villi invade into the myometrium.
- Percreta: villi penetrate through the serosa, sometimes into the bladder (hematuria) or bowel.
Consequences and management. With no cleavage plane the placenta fails to separate, and attempts at manual removal cause massive hemorrhage and DIC. Ultrasound findings such as placental lacunae and loss of the hypoechoic retroplacental clear zone raise suspicion antenatally, with MRI for mapping invasion. Management is planned cesarean hysterectomy, leaving the placenta in place.
Antepartum bleeding: previa, vasa previa and abruption
| Feature | Placenta previa | Vasa previa | Abruption |
|---|---|---|---|
| Lesion | Placenta over or near the internal os | Fetal vessels in membranes over the os | Normally sited placenta separates early |
| Bleeding | Painless, bright red | Painless, at membrane rupture | Painful, dark, may be concealed |
| Uterus | Soft, nontender | Soft, nontender | Rigid, tender, hypertonic |
| Whose blood | Maternal | Fetal | Maternal |
| Fetus | Usually stable | Sudden bradycardia or sinusoidal tracing | Distress from lost exchange surface |
| Key associations | Prior cesarean, multiparity, multiples, older age, smoking | Velamentous insertion, succenturiate lobe, IVF | Hypertension, cocaine, smoking, trauma, decompression |
Placenta previa. The placenta covers the internal os, or is low-lying when its edge lies within 2 cm of it. As the lower uterine segment develops and stretches, the attached placenta shears off its bed and bleeds painlessly, classically in the third trimester, with a soft, nontender uterus and usually a normal fetal heart rate. Risk factors include prior cesarean, multiparity, multiple gestation, advanced maternal age and smoking. Previa over a cesarean scar is the setup for accreta.
Never perform a digital cervical exam in third-trimester bleeding until ultrasound has excluded previa; a finger through the os can provoke torrential hemorrhage.
Vasa previa. Fetal vessels unprotected by cord or placenta run through the membranes across the internal os, usually because of velamentous cord insertion (vessels inserting into the membranes rather than the placental disc) or a succenturiate (accessory) lobe; IVF pregnancies are at higher risk. When the membranes rupture the vessels tear, producing modest painless bleeding with sudden fetal bradycardia or a sinusoidal tracing while the mother remains stable. The term fetus has only a few hundred milliliters of blood, so fetal mortality is high unless the condition is known in advance and delivery is by planned cesarean. The Apt test identifies fetal hemoglobin, which resists alkali denaturation.
Placental abruption. Premature separation of a normally implanted placenta creates a retroplacental hematoma. Bleeding is painful and often dark; if blood is trapped behind the placenta it may be concealed, so shock can exceed visible loss. The uterus is tender and hypertonic with frequent contractions, and the fetus becomes hypoxic. Maternal hypertension and preeclampsia are the leading risk factors; others are cocaine (acute vasoconstriction and hypertension), smoking, abdominal trauma (deceleration shear in car crashes), prior abruption and sudden uterine decompression (membrane rupture with polyhydramnios, delivery of a first twin).
Coagulopathy. Damaged decidua releases tissue factor (thromboplastin) into the maternal circulation, making abruption a leading obstetric cause of DIC, with low fibrinogen and platelets and high D-dimer. Blood dissecting into the myometrium produces a bluish, poorly contracting Couvelaire uterus that adds atony to the bleeding.
Late-pregnancy fibrinogen is normally elevated, so a fibrinogen level that looks normal for a nonpregnant adult may already reflect consumption.
Postpartum hemorrhage
Definition. Postpartum hemorrhage is a cumulative blood loss of at least 1,000 mL, or bleeding with signs of hypovolemia, within 24 hours of birth. Its causes are summarized as the 4 T's.
| Cause | Examples | Clues |
|---|---|---|
| Tone | Uterine atony (~70–80% of cases) | Soft, boggy uterus above the umbilicus |
| Trauma | Cervical, vaginal or perineal lacerations; hematoma; uterine rupture; uterine inversion | Bleeding despite a firm fundus |
| Tissue | Retained placental fragments; accreta spectrum | Missing cotyledon or torn vessel at the membrane edge |
| Thrombin | DIC, HELLP, von Willebrand disease, anticoagulants | Oozing from IV sites and wounds; blood that will not clot |
Atony. After delivery, contraction of interlacing myometrial fibers clamps the spiral arteries of the placental bed. When the myometrium fails to contract, the uterus is soft, enlarged and boggy. Risk factors are overdistension (twins, polyhydramnios, macrosomia), prolonged or very rapid labor, prolonged oxytocin exposure, chorioamnionitis, grand multiparity, magnesium sulfate and other tocolytics, and halogenated anesthetics. First steps are bimanual uterine massage and uterotonics, starting with oxytocin; methylergonovine is avoided in hypertension and carboprost (15-methyl PGF2α) in asthma.
Trauma. Continued bleeding from a well-contracted uterus points to lacerations of the cervix, vagina or perineum, a vulvar or vaginal hematoma, or uterine rupture. Uterine inversion, often after excessive cord traction on a fundal placenta, presents with a fundus that cannot be palpated abdominally, a mass at the introitus and shock out of proportion to visible bleeding.
Tissue and thrombin. The delivered placenta is inspected: a missing cotyledon, or a vessel running to a torn membrane edge that signals an unseen succenturiate lobe, means tissue remains and keeps the uterus from contracting. Coagulopathy arises from DIC (abruption, amniotic fluid embolism, sepsis, prolonged fetal demise), HELLP syndrome, von Willebrand disease or anticoagulants. Bleeding from IV sites and wounds alongside uterine bleeding means coagulopathy, not just a uterine problem.
Obstetric catastrophes
Amniotic fluid embolism. During labor, delivery or shortly after, amniotic fluid and fetal cells enter the maternal circulation and provoke an anaphylactoid response with mediator and complement activation. Acute pulmonary vasospasm and hypertension cause right heart failure, then abrupt hypoxia, hypotension and cardiovascular collapse, often with seizures. Because amniotic fluid is rich in tissue factor, DIC follows rapidly, which helps distinguish it from massive pulmonary thromboembolism. Autopsy shows fetal squamous cells, lanugo and mucin in maternal pulmonary vessels (fat globules instead suggest fat embolism after long-bone fracture).
Uterine rupture. The risk is greatest after a prior classical (vertical fundal) cesarean or a myomectomy that entered the cavity, so labor is avoided after these; it is much lower after a low transverse incision. The most common first sign is abrupt deterioration of the fetal heart rate, followed by loss of fetal station (the presenting part recedes), new abdominal pain, cessation of contractions, fetal parts palpable through the abdominal wall, hemorrhage and shock. Treatment is emergency laparotomy and delivery.