Interventions for treating placental abruption

To assess the effectiveness and safety of any intervention for the care of women and/or their babies following a diagnosis of placental abruption.

The placenta is attached to the baby by the umbilical cord, and to the inside of the uterus. If the placenta starts separating from the uterus before the baby is born, it is called placental abruption. It can be caused by a medical problem or physical trauma. This quickly becomes life‐threatening for women and babies, and cannot be repaired. The baby may need to be delivered immediately, by caesarean section if alive, and often vaginally if the baby has died. Additional treatments include pain relief, blood transfusion and monitoring. However, the review found no trials to show which treatments are best.

There is no evidence from trials to show the best way to help pregnant women and babies when there is a placental abruption.

Background

Placental abruption and placenta praevia are the two major causes of antepartum haemorrhage ‐ vaginal bleeding during the second half of pregnancy. Placenta praevia is a placenta that is situated unusually low in the uterus, and is discussed in a separate Cochrane review (Neilson 2003). Placental abruption is the premature separation of a normally sited placenta, from its attachment to the uterus. Placental abruption is a recognised cause of maternal death (Lewis 1998), especially in resource‐poor settings in low‐income countries (Prual 2000), and of death of the baby ‐ either because of sudden hypoxia or because of premature delivery. Abruption has been estimated to occur in 6.5 pregnancies per 1000 births, with an associated perinatal mortality rate of 119 per 1000 (compared to 8.2 per 1000 overall in the reference US population) (Ananth 2001a). Placental abruption is twice as common in twin, than singleton, pregnancies (Ananth 2001b).

There are independent associations of placental abruption with other conditions. These include severe fetal growth restriction, prolonged rupture of the membranes, chorioamnionitis (infection of placenta and membranes), hypertension (including pre‐eclampsia, non‐proteinuric pregnancy‐induced hypertension, and pre‐existing hypertension), cigarette smoking, advanced maternal age, and unmarried status (Kramer 1997). There is also evidence to link the use of ‘crack’ cocaine to placental abruption (Miller 1995). Trauma, notably road traffic accidents, may also cause abruption.

Although often considered a ‘non‐recurring’ obstetric complication, the risk of placental abruption was found, in one Swedish study, to rise 10‐fold in subsequent pregnancies, to 4% to 5% (Karegard 1986).

Because of the association of placental abruption with hypertensive disease during pregnancy, interventions which might help prevent high blood pressure or the sequelae of hypertension might, in theory, decrease the chances of abruption ‐ this possibility is explored in other Cochrane reviews (e.g. Abalos 2007; Duley 2005; Duley 2007; Hofmeyr 2006).

This review, in contrast, assesses treatments for placental abruption, rather than potential preventative measures. It is worthwhile to consider the clinical features of the condition to identify potential opportunities for useful treatment.

Placental abruption may or may not be associated with obvious vaginal bleeding; that is, the bleeding may be ‘revealed’ or ‘concealed’. Pain over the uterus is a prominent feature. Uterine contractions may start and cause additional, intermittent, pain. Faintness and collapse can occur, as may signs of shock. Typically, the uterus is extremely hard and tender, and it does not relax; fetal parts are difficult to palpate and the fetal heart will be inaudible if death has occurred.

Placental abruption can be a self‐extending process with the accumulating blood clot causing more separation, and thus more haemorrhage, until the edge of the placenta is reached. After this, blood can escape through the potential space between the chorion (placental membrane) and the decidua (lining of the uterus during pregnancy) until it reaches the cervix. Blood can also reach the amniotic cavity (by disrupting the placenta, producing blood stained amniotic fluid) and the myometrium (causing the bruised, so‐called ‘Couvelaire uterus’). There is usually severe fetal hypoxia associated with sizeable placental separation, and sudden fetal death is common.

The major immediate maternal risk is haemorrhagic shock; kidney damage may be seen later in the forms of either acute tubular or cortical necrosis. There may also be clinical and haematological evidence of disordered blood clotting as thromboplastins are released by placental damage and coagulation factors are consumed in the enlarging retroplacental clot at a rate that is faster than the body’s ability to replace them.

Placental abruption is essentially a clinical diagnosis, determined by the features described above and confirmed by the demonstration after delivery of a retroplacental clot indenting the placental substance. Ultrasound imaging has a much smaller role than in the diagnosis of placenta praevia. In acute severe abruption, the ultrasound appearances are often unimpressive because the fresh retroplacental clot has acoustic characteristics which may be very similar to those of the placenta itself. In less severe cases in which the pregnancy continues, the clot becomes increasingly echo‐free with time, and therefore more obvious to the ultrasonographer (Nyberg 1987).

The traditional, main principles of clinical care of a woman with placental abruption include:

  1. early delivery;

  2. adequate blood transfusion;

  3. adequate analgesia for pain relief;

  4. monitoring of maternal condition;

  5. assessment of fetal condition.

Early delivery is usual. It has been recommended that, if the baby is alive and the gestation not so early as to make fetal survival extremely unlikely, delivery should be by caesarean section (Rasmussen 1996). Even if the fetus is not obviously hypoxic as a result of placental separation, the effect of the uterine contractions which almost inevitably follow abruption might further compromise the supply of oxygen to the fetus through the placenta. Contractions may also produce shearing forces and therefore the risk of further separation. If the fetus is already dead, as is often the case, it is usual to aim for vaginal delivery.

Prompt treatment and monitoring of the mother is seen as vital. Much of the blood loss from placental abruption is not revealed, and traditional teaching advises that an abruption of sufficient severity to produce fetal death merits a minimum transfusion of two units of blood to the mother.

If there is evidence of coagulopathy (decreased fibrinogen levels, decreased concentrations of platelets, and raised levels of fibrin degradation products), expert haematological input may be required. It has been suggested that high levels of fibrin degradation products might inhibit uterine contractions and make vaginal delivery difficult to achieve in some cases of severe abruption (Basu 1969) as well as contribute to atonic postpartum haemorrhage (excessive blood loss after delivery because of failure of the uterus to contract adequately).

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