Uterine atony occurs immediately after childbirth when the muscles of the uterus fail to contract effectively. The uterus must tighten down strongly to constrict the blood vessels that supplied the placenta during pregnancy. These vessels are left exposed and bleeding after the placenta detaches from the uterine wall. When the uterine muscle, called the myometrium, remains relaxed or “atonic,” this mechanical compression does not happen, leading to excessive blood loss. Uterine atony is the most common cause of postpartum hemorrhage (PPH), a life-threatening obstetric emergency responsible for a substantial number of maternal deaths globally.
Causes Related to Uterine Overstretching
One of the most common reasons the uterus fails to contract is physical overdistension, which stretches the muscle fibers past their optimal length. When the muscle fibers are excessively elongated, their ability to shorten and contract with sufficient force is compromised. This mechanical fatigue prevents the necessary clamping action required to achieve hemostasis.
Fetal macrosomia (a significantly larger-than-average infant) is a common cause of this overstretching, as the large volume forces the uterine walls to expand beyond capacity. Similarly, carrying multiple fetuses, such as twins or triplets, results in a massive increase in internal volume. The sustained stretching leaves the muscle exhausted and less responsive to contraction signals.
Another factor is polyhydramnios, the accumulation of excessive amniotic fluid. This excess fluid volume causes the uterus to swell dramatically. In all these cases, the myometrial cells have been strained too severely, diminishing their inherent contractile power and making them unable to achieve the firm, sustained tone needed to prevent bleeding.
Factors Stemming from Labor and Delivery Management
The duration and intensity of labor can directly impact the myometrium’s ability to contract after delivery by causing muscle exhaustion. A prolonged labor (dystocia) means the uterine muscle has been working hard for an extended period. This relentless effort leads to functional fatigue, where the muscle lacks the responsiveness needed for the final, sustained contraction. Conversely, a very rapid or precipitous labor can also overwhelm the muscle fibers due to sudden, intense effort.
High parity (having had many previous births) may also cause a decline in muscle tone responsiveness over time. With each successive delivery, the myometrium may become less efficient at achieving a firm, contracted state.
Beyond physical exhaustion, certain medical interventions used during labor can directly interfere with muscle function. Pharmacological agents designed to relax smooth muscle can inadvertently affect the uterus. Magnesium sulfate, often administered to manage preeclampsia, is a powerful muscle relaxant that diminishes the uterus’s ability to contract. General anesthesia can also have a relaxant effect on the myometrium.
The hormone oxytocin is routinely used to induce or augment labor, but its mismanagement can paradoxically contribute to atony. If oxytocin is administered for a prolonged period or at high doses, the uterine muscle cells can become desensitized to the hormone. This receptor downregulation means that when a strong oxytocin response is needed after delivery, the muscle may not react appropriately, resulting in inadequate contraction.
Internal Impediments to Uterine Contraction
The presence of material inside the cavity can physically or chemically block effective contraction, even if the uterine muscle is healthy. The contraction process is obstructed if any part of the placenta remains attached. Retained placental fragments or membranes act as a physical barrier, preventing the muscle fibers from interlocking and closing the vessels completely. These fragments hold the uterine walls apart, inhibiting the mechanical closure of the bleeding site and contributing to hemorrhage.
Another significant impediment is infection within the uterine environment, most commonly chorioamnionitis (an infection of the amniotic fluid and fetal membranes). This infection creates an inflammatory state within the uterine wall, which impairs the muscle’s normal physiological response. The presence of infection can interfere with the signaling pathways that coordinate myometrial contraction, leading to poor tone.
Pre-existing structural issues within the uterus, such as large uterine fibroids (leiomyomas), can also mechanically interfere with the contraction process. Fibroids are benign growths of muscle tissue that distort the uterine cavity and wall. If a fibroid is large or located near the placental attachment site, it prevents the uniform and symmetrical contraction of the surrounding muscle. The irregular structure caused by the fibroid means the muscle cannot efficiently shorten and tighten to compress the blood vessels, regardless of hormonal stimulation or muscle health.