Uterine rupture occurs in 0.2% to 1.8% of patients with one or more previous low-segment transverse cesarean sections and in 4% to 9% of patients with a prior uterine active segment incision (classical cesarean or T-incision). One third of prior classical cesarean scar rupture occurs before the onset of labor.

Significant risk factors include:

Other situations that may increase the risk of uterine rupture but not as significantly include:

Fetal bradycardia is clinically manifested in 33% to 70% of cases. Fetal distress may be the initial presentation in catastrophic uterine rupture. In more subtle cases, the
initial presentation may be a simple rise in fetal station or change in the position for fetal heart monitor placement. Maternal signs and symptoms include hypotension, uterine tenderness, a change in uterine shape, or constant abdominal pain.

When uterine rupture is suspected, it is important to proceed emergently to laparotomy with delivery of the infant and repair of the uterine rupture. Rates of recurrent rupture in subsequent pregnancies carried to term approach 22%. Recommendations are for early delivery via cesarean section by 36 weeks.

Risk factors include ruptured membranes, unengaged fetal presenting part (including disengagement), malpresentation (breech, transverse, oblique), prematurity, multiple gestation (second twin), multiparity, and polyhydramnios.

If the cord is felt on vaginal examination, elevate the presenting part to relieve pressure on the cord, call for help, and move to the operating room for emergent cesarean section.

Appropriate anesthesia should be administered in the operating room and the viability of the fetus confirmed before proceeding with cesarean section.

Placing the patient in Trendelenburg or knee-chest position may relieve cord compression with prolapse, but the vaginal hand should continue to elevate the presenting part. This should not delay transportation to the operating room.

The interval between cord prolapse and delivery is the major predictor of newborn status. If delivered expeditiously, the neonatal outcomes are generally favorable. A cord gas should be obtained at the delivery to assess the degree of hypoxia.

Approximately 1 in 20,000 singleton pregnancies is complicated by AFE.

Mortality is around 25% in the United States, much lower than the typically reported 60% to 80%. AFE accounts for 10% of maternal deaths in the United
States. Severe neurologic deficits occur in a high percentage of survivors. Neonatal survival is reported at 70%.

Approximately 65% of AFE occurs before delivery. Emergent delivery is required for both fetal and maternal benefits.

The patient should be intubated and aggressively resuscitated.

Administer intravenous (IV) fluids, inotropic agents, and pressors to maintain adequate blood pressure. Packed red blood cells (PRBC) and fresh frozen plasma (FFP) should be available, as there is a high risk for disseminated intravascular coagulation (DIC). Factor VII has been used in cases of severe DIC. Despite all efforts, significant maternal morbidity and mortality remain high.

PPH is the leading cause of maternal death, accounting for at least 25% of maternal deaths worldwide. It is the second leading cause of pregnancy-related death in the United States, accounting for 17% of maternal mortality.

Patients often tolerate loss of up to 20% of blood volume before symptoms of hypovolemia develop (see Chapter 3). Prompt, even anticipatory, action is crucial.
Blood flow to the gravid uterus is 600 to 900 mL/min; patients can become unstable rapidly.

Establish large-bore IV access. Initiate IV fluid resuscitation. Administer supplemental oxygen and order cross-matched blood. After these initial steps, examine the patient to determine the underlying cause and address the problem expeditiously.

Blood transfusion should be considered after 1 to 2 L EBL and may be initiated earlier if bleeding is expected to continue or the patient is symptomatic.

Coagulation factors (FFP and cryoprecipitate) and platelets should be repleted with massive blood loss. Historically, one unit of FFP was given for every 4 to 6 units of PRBC to reduce dilutional and citrate coagulopathy as every 500 mL red cells is expected to dilute coagulation factors by 10%. Additionally, platelets were transfused when the platelet count dropped below 50,000/mL or after 6 to 10 units of red cell transfusion. More recent evidence suggests better outcomes with a protocol of 1:1:1 repletion of PRBC, FFP, and platelets when bleeding is ongoing or massive transfusion (>8 units of PRBC) is needed. In the operative setting, direct manual aortic compression can decrease pulse pressure and slow active bleeding to allow hemodynamic stabilization before proceeding with definitive management.

Factor VII infusion may be considered in extreme cases of hemorrhage with DIC.