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Summary Table

Category	Details
Risk Factors	Chronic hypertension, preeclampsia, prior abruption, trauma (motor vehicle accident, domestic violence), cocaine/amphetamine use, cigarette smoking, advanced maternal age, multiparity, premature rupture of membranes, short umbilical cord, uterine leiomyoma
Etiology	Premature separation of a normally implanted placenta from the uterine wall after 20 weeks of gestation, triggered by rupture of maternal spiral arteries into the decidua basalis
Patient Presentation	Painful vaginal bleeding in the third trimester, often accompanied by uterine tenderness and contractions; may present with little or no visible bleeding if the hemorrhage is concealed
Classic Physical Exam	Rigid, "board-like" uterus with continuous tenderness on palpation; dark red vaginal bleeding; signs of maternal hemodynamic instability (tachycardia, hypotension); fetal heart rate abnormalities (late decelerations, bradycardia)
Key Diagnostic Results	Clinical diagnosis supported by non-reassuring fetal heart tracing; ultrasound has low sensitivity but may show retroplacental clot; labs reveal dropping hemoglobin, elevated fibrin degradation products, low fibrinogen, and prolonged PT/PTT in severe cases
Management	Emergent cesarean delivery for maternal or fetal instability; vaginal delivery if mother and fetus are both stable and near term; aggressive IV fluid resuscitation and blood product replacement; continuous fetal monitoring
Keywords	"Painful third-trimester bleeding," "board-like uterus," "cocaine use in pregnancy," "dark blood," "concealed hemorrhage," "tetanic uterine contractions"

1. Pathophysiology

Placental abruption begins with hemorrhage into the decidua basalis, the maternal layer where the placenta anchors to the uterine wall. The bleeding originates from ruptured maternal spiral arteries, which creates a retroplacental hematoma. As this hematoma expands, it progressively shears the placenta away from its implantation site.

The clinical consequences follow directly from this mechanism. The expanding clot compresses the overlying placental tissue and reduces the functional surface area for gas exchange. This is why the fetus develops hypoxia and non-reassuring heart tracings even before the mother shows overt hemodynamic compromise. The fetal distress is often out of proportion to the visible bleeding, a concept that test-writers exploit frequently.

The uterus responds to the retroplacental blood by becoming irritable and contracting. In moderate to severe cases, blood infiltrates through the myometrium, producing the classic "board-like" or "woody" uterus (also called Couvelaire uterus when the blood dissects through the entire myometrial wall to the serosa). This tetanic contraction pattern is what distinguishes abruption from other causes of antepartum hemorrhage.

A critical downstream complication is disseminated intravascular coagulation (DIC). The damaged placental tissue releases large amounts of tissue thromboplastin into the maternal circulation, which triggers the extrinsic coagulation cascade. Widespread consumption of clotting factors and platelets follows. This is why severe abruption can present with uncontrollable bleeding from IV sites, gingival oozing, and laboratory evidence of coagulopathy. The risk of DIC is proportional to the degree of placental separation, and it develops in roughly 10% of clinically apparent abruptions but in up to 30% of severe cases.

The hemorrhage can track in two directions. If blood dissects downward toward the cervical os, the patient presents with revealed (external) hemorrhage, which is visible as vaginal bleeding. If the blood is trapped behind the placenta with intact membranes and a closed cervix, the hemorrhage is concealed. Concealed abruption is more dangerous because the degree of maternal blood loss and fetal compromise is grossly underestimated by the clinical appearance. Approximately 20% of abruptions are concealed.

2. Classification and Clinical Manifestation

Grade	Severity	Vaginal Bleeding	Uterine Findings	Fetal Status	Coagulopathy	Maternal Hemodynamics
Grade 0	Asymptomatic	None or minimal	No tenderness	Normal	Absent	Stable
Grade 1 (Mild)	~40% of cases	Mild, dark red	Mild tenderness, no rigidity	Normal heart tracing	Absent	Stable; fibrinogen > 250 mg/dL
Grade 2 (Moderate)	~45% of cases	Moderate, may be concealed	Tender, increased tone, frequent contractions	Non-reassuring (late decelerations)	Mild (fibrinogen 150-250 mg/dL)	Tachycardia, orthostatic changes
Grade 3 (Severe)	~15% of cases	Severe or concealed with shock	Board-like rigidity, tetanic contractions	Fetal demise common	Overt DIC (fibrinogen < 150 mg/dL)	Hypotension, hemorrhagic shock

Grade 0 is diagnosed retrospectively when a retroplacental clot is found on inspection of the delivered placenta. It carries no clinical significance at the time of delivery but is relevant because it identifies patients at increased risk for recurrence in future pregnancies.

The distinction between Grade 2 and Grade 3 is the most testable boundary. Fetal demise and overt coagulopathy are the hallmarks that push a case into Grade 3. When a vignette describes a patient with painful bleeding, a rigid uterus, absent fetal heart tones, and oozing from venipuncture sites, the answer is severe abruption with DIC until proven otherwise.

3. Diagnostic Workup

Test	Role	Key Findings
Clinical assessment	Best initial approach	Painful bleeding + uterine rigidity + fetal distress = presumptive diagnosis
Continuous fetal monitoring	Immediate, concurrent	Late decelerations, decreased variability, bradycardia
CBC	Baseline and serial	Hemoglobin may be normal initially (hemoconcentration), then drops; thrombocytopenia in severe cases
Coagulation panel (PT, PTT, fibrinogen, D-dimer)	Assess for DIC	Fibrinogen < 200 mg/dL is concerning; < 150 mg/dL indicates severe coagulopathy
Type and crossmatch	Preparation for transfusion	Always ordered in any suspected abruption
Transabdominal ultrasound	Supportive but not required for diagnosis	May show retroplacental hypoechoic collection; sensitivity only 25-50%
Kleihauer-Betke test	Assess fetomaternal hemorrhage	Positive in Rh-negative mothers to guide RhoGAM dosing

Placental abruption is a clinical diagnosis. This is the single most important concept for exam purposes. You do not wait for imaging confirmation before acting. A patient who presents with painful vaginal bleeding, a tender hypertonic uterus, and fetal heart rate abnormalities has abruption until proven otherwise.

Ultrasound is often ordered but has poor sensitivity (approximately 25-50%) for detecting retroplacental hemorrhage. A negative ultrasound does not rule out abruption. The primary utility of ultrasound in this setting is to exclude placenta previa, which is the main differential for third-trimester bleeding. If ultrasound shows a normally positioned placenta and the clinical picture fits, the diagnosis is abruption regardless of whether a clot is visualized.

Fibrinogen is the single most useful lab value for gauging severity. In normal pregnancy, fibrinogen is physiologically elevated (300-600 mg/dL). A fibrinogen level that appears "normal" at 200 mg/dL in a pregnant patient is actually abnormally low and signals evolving coagulopathy. A level below 150 mg/dL predicts a high likelihood of progression to clinically significant DIC. Serial fibrinogen trending is more informative than a single value.

The Kleihauer-Betke test detects fetal red blood cells in the maternal circulation. It does not diagnose abruption, but it quantifies the degree of fetomaternal hemorrhage. This is important in Rh-negative mothers because the standard dose of RhoGAM (300 mcg) covers only 30 mL of fetal whole blood. If the Kleihauer-Betke indicates a larger volume of fetomaternal transfusion, additional doses are required.

4. Management and Treatment

Clinical Scenario	Management
Mild abruption, preterm (< 34 weeks), stable mother and fetus	Hospitalize, continuous monitoring, betamethasone for fetal lung maturity (12 mg IM x 2 doses, 24 hours apart), tocolysis is controversial and generally avoided
Moderate abruption, any gestational age, non-reassuring fetal status	Emergent cesarean delivery, concurrent resuscitation
Severe abruption with fetal demise	Vaginal delivery preferred if maternal coagulation is manageable; aggressive correction of DIC with blood products
Severe abruption with live fetus	Emergent cesarean delivery
Any abruption with maternal hemodynamic instability	Large-bore IV access x 2, crystalloid resuscitation, packed red blood cells, fresh frozen plasma, cryoprecipitate if fibrinogen < 150 mg/dL, platelets if < 50,000
Rh-negative mother	RhoGAM 300 mcg IM within 72 hours; Kleihauer-Betke to determine if additional doses are needed

The first priority in any suspected abruption is maternal stabilization and continuous fetal monitoring. Two large-bore (16-18 gauge) IV lines should be placed immediately, and crystalloid resuscitation initiated. A type and crossmatch should be sent without delay because the need for transfusion can escalate rapidly.

The decision between cesarean and vaginal delivery depends on two factors: fetal viability and maternal stability. If the fetus is alive and showing non-reassuring tracings, emergent cesarean is indicated because prolonged labor exposes the fetus to worsening hypoxia. If fetal demise has already occurred, vaginal delivery is preferred because it avoids surgical morbidity in a patient who may already have DIC. Performing a cesarean on a coagulopathic patient dramatically increases the risk of uncontrollable surgical hemorrhage.

For the preterm fetus (less than 34 weeks) with a mild abruption where both mother and fetus are stable, expectant management with close inpatient monitoring is reasonable. Betamethasone (12 mg intramuscularly, two doses given 24 hours apart) should be administered for fetal lung maturation. Tocolysis is generally contraindicated in the setting of abruption because suppressing contractions may mask worsening separation and delay necessary delivery. This is a commonly tested point.

DIC management follows the standard approach of replacing what is consumed. Fresh frozen plasma (FFP) replaces clotting factors and is given when PT/PTT are prolonged. Cryoprecipitate is the targeted treatment for hypofibrinogenemia (each unit raises fibrinogen by approximately 5-10 mg/dL; a typical dose is 10 units). Platelet transfusion is indicated when the count falls below 50,000/mcL in the setting of active bleeding.

If the uterus fails to contract adequately after delivery due to myometrial infiltration by blood (Couvelaire uterus), uterotonics such as oxytocin (10-40 units in 1 L of normal saline), methylergonovine (0.2 mg IM, contraindicated in hypertension), or carboprost (250 mcg IM, contraindicated in asthma) are administered. Refractory postpartum hemorrhage may require uterine artery embolization, B-Lynch compression suture, or ultimately hysterectomy.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Is Similar	Key Discriminator
Placenta previa	Third-trimester vaginal bleeding; both are obstetric emergencies	Previa presents with painless, bright red bleeding and a soft, non-tender uterus; diagnosed by ultrasound showing placenta covering the internal os
Vasa previa	Vaginal bleeding at or near rupture of membranes; fetal distress	Bleeding onset coincides with rupture of membranes; fetal heart rate drops rapidly; diagnosed by Apt test showing fetal blood
Uterine rupture	Sudden abdominal pain, vaginal bleeding, fetal distress	History of prior cesarean scar; loss of uterine contour on palpation; fetal parts palpable outside the uterus; occurs during active labor
Preterm labor	Uterine contractions, possible vaginal bleeding	Contractions are regular and intermittent (not constant); uterus relaxes between contractions; cervical change is present; no rigidity
Preeclampsia with HELLP	Can coexist with abruption; thrombocytopenia, elevated LDH	HELLP presents with right upper quadrant pain, elevated liver enzymes, and hemolysis (schistocytes on smear); no retroplacental pathology
Cervical or vaginal laceration	Vaginal bleeding, sometimes after trauma or intercourse	Uterus is soft and non-tender; fetal heart tracing is normal; bleeding source identified on speculum exam

The single most important differential to distinguish is placenta previa vs. abruption. Both present with third-trimester bleeding. The discriminators are pain and uterine tone. Abruption is painful with a rigid uterus. Previa is painless with a soft uterus. A digital cervical exam is contraindicated in any patient with third-trimester bleeding until previa has been excluded by ultrasound, because palpating a previa can trigger catastrophic hemorrhage.

6. Traps and High-Yield Pearls

The most common trap on this topic is the concealed hemorrhage vignette. A patient presents with severe abdominal pain, a rigid uterus, fetal bradycardia, and tachycardia with hypotension, but only minimal or no vaginal bleeding. Students who anchor on "third-trimester bleeding" as the defining feature of abruption will miss the diagnosis when the hemorrhage is hidden. The amount of visible bleeding does not correlate with the severity of the abruption. If the clinical picture shows uterine rigidity and fetal distress, treat it as abruption regardless of how much blood is seen externally.

The second major trap involves cocaine use. A vignette describing a young pregnant woman with sudden-onset abdominal pain after using cocaine is pointing toward abruption. Cocaine causes intense vasospasm of the uterine arteries, which leads to ischemia and premature placental separation. Students may be distracted by the substance use history and consider alternative diagnoses, but cocaine-associated abruption is one of the most classic exam associations.

A third testing angle is the "normal" fibrinogen trap. Because fibrinogen is physiologically elevated in pregnancy, a value of 200 mg/dL looks reassuring to someone reading it against non-pregnant reference ranges. In a pregnant patient, this value is low and signals early DIC. Always interpret labs in the context of pregnancy physiology.

Finally, remember that ultrasound does not rule out abruption. A negative ultrasound in a patient with a convincing clinical presentation should not change your management. This diagnosis is made at the bedside, not in the radiology suite. The core competency being tested is the ability to recognize the clinical triad (painful bleeding, uterine rigidity, fetal distress), initiate resuscitation immediately, and make a delivery decision based on maternal and fetal status rather than waiting for confirmatory imaging.

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