Uterine Atony
The most common cause of PPH is uterine atony. Patients at increased risk for uterine atony include those with high parity, overdistended uterus (e.g., multiple gestation, polyhydramnios), prolonged or rapid labor, use of oxytocin for induction or augmentation, and use of magnesium sulfate. Uterine tone can usually be assessed by abdominal palpation after delivery; even when uterine tone seems normal, initial treatment for PPH is frequently directed toward uterine atony. However, when initial management efforts fail, the obstetrician should not waste time treating presumed uterine atony before evaluating other potential causes of hemorrhage.
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Laceration
Lacerations of the perineum, vagina, cervix, or uterus may result in visible or concealed hemorrhage. Careful examination of the birth canal, including both inspection and palpation, is necessary to eliminate laceration as a source of PPH.
The obstetrician should also be aware of the potential of uterine rupture to cause massive hemorrhage. Although uterine rupture occurs most often with a prior uterine scar, it can occur spontaneously. High parity, oxytocin use, and obstetric procedures (e.g., forceps, breech delivery) are risk factors for uterine rupture. The increasing frequency of vaginal birth after cesarean section makes it important to consider uterine rupture in all cases of hemorrhage in this population.
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Retained Placenta
Retained placenta causes uterine atony by preventing uterine contraction, which compresses the myometrial spiral arteries. Retained products may cause delayed PPH by interfering with involution of the placental site. At the time of delivery, the maternal surface of the placenta should be carefully inspected to ensure that no fragments are missing. The fetal surface is then examined, with particular attention to the margins to look for severed blood vessels that may have led to a succenturiate placental lobe. Routine uterine exploration to rule out retained products is uncomfortable for the patient and may increase the risk of postpartum infection; however, if doubt exists about the potential for retained products, uterine exploration is appropriate.
Placenta Accreta
Placenta accreta occurs when placental villi attach directly to or invade the myometrium, preventing normal placental separation. Placenta accreta is commonly associated with placenta previa (64% of placenta accreta) or a history of prior cesarean section, dilatation and curettage, or abortion. An anterior placenta previa in a patient with prior cesarean section should make the obstetrician particularly wary of an accreta.6 Accreta should be considered whenever a retained placenta occurs or when manual removal of the placenta is particularly difficult. Although most cases of accreta require hysterectomy, some patients can be managed with curettage, suture of the bleeding site, or hypogastric artery ligation. Modern management of this complication is credited with reducing the maternal mortality rate in this condition from 37% to 3%.7
Coagulopathy
Immediate hemostasis after delivery occurs by uterine compression of myometrial spiral arteries. However, most coagulopathies (e.g., idiopathic thrombocytopenic purpura, von Willebrand’s disease) may also cause PPH. Disseminated intravascular coagulation from abruptio or severe preeclampsia may also result in PPH. Coagulopathies have the potential to cause PPH up to several days after delivery.8 Although the obstetrician is usually aware of these problems before delivery, there is a potential for a coagulopathy to make its initial presentation as PPH.
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Uterine Inversion
Uterine inversion has been reported in the past to be extremely rare (1:20,000 deliveries) and to have an associated high mortality rate.9 Recent studies suggest that the rate of uterine inversion is approximately 1:2000.10, 11 The high mortality rate of uterine inversion in the past may have resulted from the practice of not performing routine vaginal and cervical examination immediately postpartum.12 The major complication of uterine inversion is PPH. Shock is directly related to the volume of blood lost.10, 11
Uterine inversion can occur spontaneously but usually is associated with uterine fundal pressure and cord traction to deliver the placenta. Primiparity, uterine hypotonia, and fundal placental implantation are associated with an increased risk of uterine inversion. A 10-year review of uterine inversions at the University of Michigan, from 1970 to 1980, revealed 10 uterine inversions, with an incidence of 1:1770 deliveries (Table 1). The degree of shock was related to hemorrhage. In all of the cases the uterus was replaced manually. Immediate recognition of uterine inversion and prompt replacement appear to be the keys to preventing death and complications.
Table 1. Cases of uterine inversion, University of Michigan, 1970-1980
Late Postpartum Hemorrhage
Late (or secondary) PPH is defined as hemorrhage occurring more than 24 hours after delivery. Causes include subinvolution of the placental site, retained products, lacerations, and coagulopathy.13, 14 Although infection is occasionally noted with delayed PPH, it is uncommon. The management of delayed PPH follows the same sequential process as that of early PPH.
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