Primary Postpartum Hemorrhage (PPH)

Summary

Primary postpartum hemorrhage (PPH), occurring within 24 hours of delivery, is a leading cause of maternal death, most often due to uterine atony. Other causes are summarized as the “5 T’s”: Tone, Tissue, Trauma, Thrombin, and Traction. Diagnosis is clinical with supportive imaging and labs, while management requires rapid resuscitation, uterotonics, tranexamic acid, and escalation to surgical measures if bleeding persists. Prevention relies on antenatal risk assessment and active management of the third stage of labor.

Definition

Postpartum hemorrhage (PPH) is defined as blood loss of ≥500 mL after vaginal delivery or ≥1000 mL after cesarean section, or any blood loss associated with hemodynamic instability.

• Primary PPH: blood loss within the first 24 hours postpartum (most common).

• Secondary PPH: blood loss occurring between 24 hours and 12 weeks postpartum.

Epidemiology

PPH complicates approximately 5% of deliveries and remains the leading cause of maternal mortality worldwide, accounting for about 12% of maternal deaths in the United States. Primary PPH is responsible for the majority of cases, with uterine atony implicated in up to 80%.

Etiology – The 5 T’s

The causes of PPH can be summarized by the “5 T’s”:

1. Tone (uterine atony) – inadequate myometrial contraction, most common cause.

2. Tissue (retained products of conception or abnormal placentation).

3. Trauma (lacerations, hematomas, uterine rupture, inversion).

4. Thrombin (coagulopathies or clotting disorders).

5. Traction (uterine inversion from cord traction or fundal pressure).

1. Uterine Atony

• Risk factors: overdistension (polyhydramnios, multiple gestation, macrosomia), prolonged labor, prolonged oxytocin use, multiparity, chorioamnionitis, uterine fibroids, maternal obesity, and general anesthesia.

• Clinical features: profuse vaginal bleeding with a soft, enlarged, “boggy” uterus.

• Management: uterine massage, bladder emptying, bimanual compression, and sequential use of uterotonics (IV oxytocin → methylergonovine if no hypertension → carboprost if no asthma → misoprostol if others unavailable). Tranexamic acid should be administered early. If bleeding persists, consider intrauterine balloon tamponade, compression sutures (B-Lynch), arterial ligation, embolization, or hysterectomy.

2. Retained Placenta / Abnormal Placentation

• Risk factors: placenta previa, placenta accreta spectrum, prior uterine surgery, multiparity, advanced maternal age, assisted reproduction.

• Clinical features: failure of complete placental separation, ongoing bleeding, or ultrasonographic evidence of retained tissue.

• Management: manual removal under anesthesia, suction curettage, uterine tamponade, or hysterectomy for placenta accreta spectrum.

3. Trauma (Genital Tract Injuries)

• Causes: cervical or vaginal lacerations (often forceps/assisted delivery), episiotomy, puerperal hematomas, or uterine rupture.

• Clinical features: persistent bleeding despite a contracted uterus, genital tract pain, visible hematomas, or hemodynamic collapse.

• Management: surgical repair of lacerations, incision and drainage of hematomas, arterial embolization or ligation, laparotomy for rupture, and hysterectomy if conservative measures fail.

4. Uterine Inversion

• Causes: excessive cord traction, fundal pressure, placenta accreta, fetal macrosomia, uterine anomalies.

• Clinical features: sudden hemorrhage, severe pain, shock out of proportion to blood loss, absence of palpable uterine fundus.

• Management: stop uterotonics, initiate resuscitation, and perform immediate manual reposition (Johnson method). Surgical correction is indicated if unsuccessful.

5. Coagulopathy (Thrombin)

• Causes: disseminated intravascular coagulation (DIC), severe preeclampsia, placental abruption, sepsis, or inherited bleeding disorders.

• Diagnosis: prolonged PT, aPTT, low fibrinogen, elevated D-dimer.

• Management: replacement of deficient factors (FFP, cryoprecipitate, platelets) alongside control of bleeding source.

Diagnosis

• Clinical: brisk vaginal bleeding, signs of hypovolemia (tachycardia, hypotension, dizziness), uterine tone assessment, and speculum examination to identify trauma or retained tissue.

• Imaging: ultrasound to detect retained tissue or abnormal placentation; Doppler or MRI when needed.

• Laboratory: hemoglobin, hematocrit, coagulation profile, fibrinogen levels.

Management – Stepwise Approach

1. Multidisciplinary team activation: obstetrician, anesthetist, midwife, and blood bank.

2. Resuscitation: oxygen, large-bore IV access, IV crystalloids, blood transfusion as indicated, continuous vital sign and urine output monitoring.

3. Assess uterus:

• Contracted → rule out trauma, tissue, or coagulopathy.

• Atonic → uterine massage, empty bladder, uterotonics, tranexamic acid.

4. Surgical options if refractory: balloon tamponade, compression sutures, arterial ligation/embolization, hysterectomy (last resort).

Prevention

• Antenatal identification and correction of anemia and coagulopathies.

• Sonographic evaluation in women with previous cesarean delivery to detect placenta accreta.

• Active management of the third stage of labor (AMTSL):

• Administration of uterotonics (oxytocin IM/IV).

• Controlled cord traction (Brandt-Andrews maneuver).

• Uterine massage and compression techniques (Credé maneuver, bimanual massage).

• Avoid unnecessary episiotomy and traumatic assisted deliveries.

Complications

• Anemia

• Hypovolemic shock

• Disseminated intravascular coagulation

• Sheehan syndrome (pituitary necrosis)

• Infection

• Thromboembolism

• Maternal death

• Rare fetal complications (e.g., with velamentous cord insertion or vasa previa)