Uterine atony is the failure of the uterus to contract adequately following delivery. Contraction of the uterine muscles during labor compresses the blood vessels and slows flow, which helps prevent hemorrhage and facilitates coagulation. Therefore, a lack of uterine muscle contraction can lead to an acute hemorrhage, as the vasculature is not being sufficiently compressed. Uterine atony is the most common cause of postpartum hemorrhage, which is an emergency and potential cause of fatality. Across the globe, postpartum hemorrhage is among the top five causes of maternal death. Recognition of the warning signs of uterine atony in the setting of extensive postpartum bleeding should initiate interventions aimed at regaining stable uterine contraction.
There are many risk factors for uterine atony and several are due to the type of labor a mother experiences such as prolonged labor, labor lasting less than 3 hours, uterine inversion, the use of magnesium sulfate infusions, and extended use of oxytocin. Uterine distention caused by things like more than one fetus present, polyhydramnios, fetal macrosomia, uterine fibroids, chorioamnionitis can also lead to decreased uterine function and atony. Retained placental tissue or placental disorders, such as an adherent placenta, placenta previa, and abruption placentae increase the mother's risk of PPH. Body mass index (BMI) above 40 and coagulopathies are known risk factors.
Magnesium sulfate is used often in patients with preeclampsia and eclampsia, can inadvertently inhibit uterine contractions. In addition, preeclampsia can lead to blood disorders such as thrombocytopenia, platelet abnormalities, and disseminated intravascular coagulation. Cesarean delivery, especially after prolonged labor, may cause the muscles of the uterus to become tired and stop contracting or contraction can be inhibited at the surgical site.
Uterine atony occurs during 1 in 40 births in the United States and is responsible for at least 80% of cases of postpartum hemorrhage.