The most common cause of postpartum hemorrhage is uterine atony, i.e. failure of the uterus to contract. Primary postpartum hemorrhage due to uterine atony occurs when the relaxed myometrium fails to constrict these blood vessels, thereby allowing hemorrhage. Since up to one-fifth of maternal cardiac output, or 1000 ml/min, enters the uteroplacental circulation at term, postpartum hemorrhage is capable of exsanguinating the mother within a short time. Whilst uterine atony is responsible for 75-90% of primary postpartum hemorrhage, traumatic causes of primary postpartum hemorrhage (including obstetric lacerations, uterine inversion and uterine rupture) comprise about 20% of all primary postpartum hemorrhage (see Chapter 9). Significant but less common causes of postpartum hemorrhage include congenital and acquired clotting abnormalities, which comprise around 3% of the total24. Uterine atony is responsible for the majority of primary postpartum hemorrhage originating from the placental bed. Although the most important risk factor is a previous history of atonic post-partum hemorrhage (relative risk 3.3)25, many other important risk factors often found in combination.
Failure of the uterus to contract may be associated with retained placenta or placental fragments, either as disrupted portions, or more rarely a succenturiate lobe. The retained material acts as a physical block against strong uterine contraction, which is needed to constrict placental bed vessels, but, in most cases, dysfunctional postpartum contraction is the primary reason for placental retention. It is more likely for the placenta to be retained in cases of atonic postpartum hemorrhage, and so the contraction failure often becomes self-perpetuating. The reasons for this contractile dysfunction are unknown. The exception is uterine fibroids, where the source of distension cannot be removed by uterine contraction, and must therefore cause the atony. However, the uterus does not even have to be distended during the third stage for contractile dysfunction to occur. Distension prior to delivery, which occurs with multiple pregnancy and polyhydramnios, also affects the ability of the uterus to contract efficiently after delivery, and is thus another risk factor for atonic postpartum hemorrhage.
When postpartum hemorrhage occurs following an antepartum hemorrhage, the scenario is particularly difficult since there have been two episodes of blood loss. A rare but serious complication of abruption is extravasation of blood into the myometrium, known as a Couvelaire uterus, which impairs the physiological uterine contraction/retraction hemostatic process. However, the relationship between the extravasation process and uterine dysfunction is not fully understood. Chorioamnionitis has a similar effect for unknown reasons. Both ante-partum hemorrhage and chorioamnionitis also impair uterine contraction during the first two stages of labor, and prolonged labor in general is a risk factor for postpartum hemorrhage. Conventional wisdom suggests that delay in the first two stages leads to uterine atony, but it is more logical to suggest that uterine dysfunction before onset of labor results in delay in all three stages, and thus causes postpartum hemorrhage. As far as we are aware, there is no ongoing research into this 'universal uterine dysfunction'.
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