1

What are the major causes of third-trimester bleeding?

A “bloody show” is the most common cause of bleeding during the third trimester. This bleeding occurs during labor and is due to effacement and dilation of the cervix. Placental problems are responsible for most pathologic bleeding in the third trimester, and placental abruption and placenta previa are the most common placental problems. Cervical bleeding secondary to polyps and carcinoma is much less common. Vasa previa, umbilical cord vessels traveling within the placental membranes and covering the cervical os, is a rare cause of third-trimester bleeding. Other rare causes of third-trimester bleeding are maternal coagulopathy, owing to preeclampsia, and intrauterine fetal demise ( Box 56-1 ).

2

What is abruptio placentae, and what are the risk factors for this condition?

Abruptio placentae refers to premature separation of the placenta (i.e., before delivery of the fetus). It occurs in about 1 in 100 to 1 in 150 deliveries and carries a perinatal mortality rate of approximately 20%. The incidence of abruption increases with age and is more common in African American women. Abruption is associated with chronic or pregnancy-induced hypertension, multiparity, cigarette smoking, and cocaine abuse. In women who have experienced a prior abruption, the risk of recurrence is 10 times higher than that of the general population.

3

What are the manifesting signs and symptoms of abruptio placentae, and how is the diagnosis made?

Classically, abruptio placentae is described as painful bleeding. The patient may experience a sudden “tearing” pain in the abdomen, followed by the onset of vaginal bleeding and labor pains. A tumultuous labor pattern follows, with frequent contractions and an increase in base tone of the uterus. The patient may state that it feels as though the contraction never ends. The amount of vaginal bleeding is variable and does not always correlate with the degree of placental separation. If the abruption is central, little vaginal bleeding may be noted because most of the bleeding is retroplacental. An increase in uterine fundal height may occur because up to 2 L of blood may collect behind the placenta. Blood extravasation into the myometrium causes the purple-colored Couvelaire uterus. Severe hemorrhage may lead to maternal hypovolemic shock, fetal distress, or fetal demise. Disseminated intravascular coagulopathy (DIC) may also occur in the face of severe abruption. and Brekke (1967) were the first to demonstrate that the retroplacental clot could not account for the degree of systemic hypofibrinogenemia seen in abruptio placentae. et al. (1985) explained how open venous sinuses beneath the detached placenta could allow thromboplastic material to enter the maternal circulation and initiate DIC.

Diagnosis of abruption is initially made by clinical evaluation. Ultrasound evaluation of the placenta may identify a retroplacental clot and separation of the placenta from the uterine wall. After delivery, examination of the placenta may reveal an adherent clot; however, the placenta may appear normal.

4

Describe the obstetric management of abruptio placentae.

The diagnosis of placental abruption usually results in a decision to deliver the fetus. If the infant is preterm, delivery may lead to neonatal complications or death. In this scenario, if the abruption is deemed to be small, without evidence of continued bleeding, and the mother remains stable (i.e., normal vital signs, stable hematocrit and clotting), conservative management with observation may be warranted. Any evidence of extension of the abruption usually leads to immediate delivery.

After a decision to deliver the fetus, preterm or term, is made, the mode of delivery, vaginal or cesarean delivery, is determined. Cesarean delivery is not always needed. If the abruption is small and there is no evidence of maternal compromise, a trial of labor, either spontaneous or induced, may be allowed. However, if there is evidence of either maternal or fetal compromise, a cesarean delivery is warranted. Management includes vigorous maternal resuscitation with fluids, blood, and blood products to treat a coagulopathy. Management is discussed in more detail in the following sections.

5

Describe the effects of pregnancy on coagulation.

Pregnancy is commonly referred to as a hypercoagulable state and is associated with an increased incidence of thrombotic disease. Pregnancy is characterized by increased levels of clotting factors, especially fibrinogen. There is an enhanced fibrinogen catabolism by thrombin, marked by increased levels of fibrinopeptide A. Platelet count may decrease or remain normal in pregnancy. et al. (1988) demonstrated no statistically significant change in platelet count during pregnancy; however, 104 of 2000 patients had platelet counts <150 × 10 ⁹ /L. et al. (1983) reported a decrease in platelet count secondary to increased platelet consumption during the last 8 weeks of gestation. Additionally, there is a dramatic short-term increase in coagulability immediately after delivery as manifested by an increase in factor V and factor VIII activity, a decrease in fibrinogen levels, and a decrease in partial thromboplastin time (PTT) ( Box 56-2 ).

6

What is disseminated intravascular coagulopathy, and how is it managed?

DIC is characterized by activation of systemic coagulation leading to consumption of clotting factors and activation of secondary fibrinolysis. This condition results in hypofibrinogenemia, thrombocytopenia, and production of fibrin degradation products. The clinical presentation is marked by hemorrhage, poor clot formation, and bleeding from all puncture sites, such as intravenous insertion sites. Abnormal laboratory values include elevation in prothrombin time (PT), PTT, low platelet count, and fibrinogen level ( Box 56-3 ).

Successful treatment of DIC requires removal of the source (i.e., delivery of the fetus and placenta). In addition to delivery, treatment of the coagulopathy with fresh frozen plasma (FFP), cryoprecipitate for fibrinogen replacement, and platelets is necessary until the process begins to reverse.

7

How is fetal distress diagnosed?

In the 1960s, continuous electronic FHR monitoring was developed to assess fetal well-being during labor. FHR monitoring can be performed directly by placing an electrode on the fetal scalp or indirectly by placing an ultrasound probe on the maternal abdomen. Characteristics of FHR patterns are divided into baseline and periodic features ( Box 56-4 ).

BOX 56-4

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