Uterine fibroids represent common benign tumors in women encountered in obstetrics and gynecology. As the average age of childbearing in women is delayed and with advances in ultrasound imaging technologies, the detection rate of uterine fibroids during pregnancy has been increasing annually. The incidence of these tumors is approximately 25% among women of reproductive age; among them, pregnant women with uterine fibroids comprise 0.5% - 1% of all fibroid patients and account for 0.65% - 3.9% of the overall pregnant population [1] . Most pregnant women with uterine fibroids are asymptomatic during pregnancy; however, the anatomical location and size of uterine fibroids can lead to different symptoms. Pain is the most frequent complication associated with uterine fibroids during pregnancy, with an incidence as high as 15%. The most common cause of pain is “red degeneration” of the fibroid or fibroid torsion [2] . The impact of concomitant uterine fibroids on pregnancy outcomes depends on factors such as fibroid size, location, type, and associated complications.

Currently, the growth characteristics of uterine fibroids during pregnancy are attracting widespread attention. However, effective studies on the growth potential of fibroids during pregnancy—a period marked by substantial changes in hormone levels and multi-organ function—remain insufficient [3] . Existing research indicates that, due to the unique hormonal milieu of pregnancy, fibroids may enlarge with increasing gestational age. Nevertheless, changes in fibroid size during gestation display a nonlinear correlation with gestational age. Following conception, elevated estrogen and progesterone bind to estrogen receptors on smooth muscle fibroid cells, effectively stimulating proliferation in vitro. As the secretion of these hormones rises during pregnancy, fibroids may enter a pronounced proliferative phase, with tumor enlargement being most notable in early and mid-pregnancy. In certain cases, giant uterine fibroids may even lead to pedicle torsion [4] . With the progression of pregnancy, expansion of the amniotic cavity and uterine growth may induce local vascular changes in the fibroid, resulting in regional ischemia that may impede fibroid growth in late gestation [5] . After delivery, following hormonal withdrawal, most enlarged fibroids tend to regress spontaneously. Regarding the present case, the patient’s fibroid was measured at approximately 4.3 cm × 3.5 cm × 4.7 cm before pregnancy. In early pregnancy, the fibroid expanded to 6.5 cm × 4.5 cm × 2.8 cm; in mid-pregnancy, it was measured at 6.3 cm × 3.9 cm; and intraoperatively in late pregnancy, no significant change in size was observed when compared to early and mid-pregnancy. Consequently, for pregnant women with uterine fibroids, special attention should be paid to fibroid changes during early and mid-gestation. For those with significant fibroid growth, prenatal management should be intensified and comprehensive assessment implemented to optimize maternal and fetal safety.

The course of labor encompasses the entire process of childbirth and is influenced by various factors, including uterine contractions and the birth canal. Studies have demonstrated that pregnancy complicated by uterine fibroids can alter the normal polarity and intensity of uterine contractions, predisposing to uterine inertia and prolonged labor [6] . During the first stage of labor, smooth muscle fibroids located in the lower uterine segment may hinder the descent and engagement of the fetal presenting part, resulting in a high floating presentation and slow cervical dilation, thereby impeding the progress of labor. In the second stage, uterine fibroids may lead to uterine inertia, causing slow descent of the fetal presenting part. Prolonged compression by the fetal head on tissues in the lower uterine segment and perineum may result in edema and overstretching of muscle fibers, further prolonging labor. Pergialiotis V et al. [7] performed a meta-analysis on the association between the duration of the second stage of labor and adverse maternal and neonatal outcomes, showing that a prolonged second stage increases the risk of complications in both mothers and neonates. This may induce secondary uterine inertia and elevate the rates of vaginal assisted delivery and cesarean section. Evidence suggests that the diameter of uterine fibroids is positively correlated with the cesarean section rate among women with uterine fibroids [8] . Retrospective studies report that women with large fibroids (diameter >5 cm) have significantly higher rates of postpartum hemorrhage and cesarean section, an increased risk of fetal malpresentation, and that intramural fibroids are particularly prone to cause postpartum hemorrhage [9] [10] . Wang Xiaoxian et al. [11] suggest that for uterine fibroids with a diameter <6 cm, vaginal delivery with moderate trial of labor may be appropriate, whereas for fibroids ≥6 cm in diameter, elective cesarean section is recommended to avoid the risks associated with failed vaginal trial of labor. However, there is currently no relevant literature or guidelines supporting this conclusion, and further clinical validation is required. Additionally, in late pregnancy, the uterus enlarges rapidly (with a volume reaching 500 - 1000 times that of the non-pregnant uterus), resulting in a shift in its center of gravity. Pedunculated subserous fibroids are susceptible to rotation or torsion due to gravity. Given that the pedicles of subserous fibroids are usually slender with a single blood supply, torsion may readily cause ischemia. If the fibroid is located on the anterior or lateral uterine wall, fetal movement or uterine contractions may further increase the risk of torsion.

In this case, the patient, a primipara, was admitted due to premature rupture of membranes and exhibited no signs of acute abdomen. Both the patient and her family strongly desired vaginal delivery. Spontaneous labor began two hours after the rupture of membranes. The first stage of labor lasted 9 hours and 30 minutes. During the second stage, secondary uterine inertia developed. Despite intravenous oxytocin administration, there was no significant progress in labor, and the descent of the fetal head was arrested. Consequently, an emergency cesarean section was performed to terminate the pregnancy. Intraoperatively, a large subserosal myoma was identified at the uterine fundus near the anterior wall; the myoma had undergone 720˚ torsion, resulting in incomplete uterine rupture. However, the patient did not show marked symptoms of acute abdomen, with no notable abdominal tenderness or rebound pain. This takes into account that after the onset of labor, the patient’s regular uterine contraction pain may mask the pain caused by tumor torsion, making it difficult for the patient to report abdominal pain as the primary complaint. This patient did not undergo painless delivery. If painless delivery had been administered, the symptoms of acute abdominal conditions would have been even more challenging to differentiate and diagnose. This underscores the need for clinicians to closely monitor the impact of fibroid size and location on the birth canal and fetus in pregnant women with uterine fibroids. Especially after the onset of labor, subserosal fibroids situated on the anterior or lateral uterine wall may have an increased risk of torsion during contractions, raising the possibility of uterine rupture due to torsion. A comprehensive assessment and timely intervention, as well as the scientific and standardized selection of delivery methods, are necessary to prevent adverse pregnancy outcomes.

Pedicle torsion of uterine fibroids is an uncommon complication, most frequently occurring when subserosal fibroids with pedicles become twisted. If not promptly managed, this condition can result in uterine rupture and pose a life-threatening risk to the patient. The incidence is notably higher among pregnant patients and those in labor, necessitating heightened clinical attention. According to the literature, subserosal fibroids with slender pedicles are predisposed to torsion arising from changes in body position or external forces [12] . During pregnancy, uterine contractions and the onset of labor can induce pedicle torsion exceeding 360˚, which interrupts blood flow, provokes further constriction, and leads to ischemic necrosis. Moreover, 6 - 12 hours following fibroid torsion, ischemic necrosis triggers the release of inflammatory mediators (IL-6, TNF-α), resulting in inflammatory infiltration of the adjacent myometrium and increasing myometrial tissue fragility [13] . Enlargement of the necrotic, edematous fibroid mass, along with traction from uterine contractions, predisposes weak areas—such as the fibroid’s attachment site—to rupture. The risk of rupture is further elevated during pregnancy due to thinning and stretching of uterine muscle fibers combined with traction and torsion [14] . Studies indicate that, given the relatively poor blood supply to the posterior uterine wall, ruptures most commonly occur in this region [15] . In the present case, the patient was found to have a subserosal uterine fibroid prior to pregnancy, which enlarged to 6 cm × 4 cm × 3 cm in late gestation. Following cesarean section and laparotomy, revealed approximately 200 ml of fresh blood with clots within the pelvic and abdominal cavities. Surgical exploration identified the fibroid exhibiting a 720˚ torsion, resulting in partial rupture of the uterine myometrium and active bleeding. The fibroid was completely resected, the wound was sutured, and hemostasis was achieved, with a favorable prognosis. Therefore, clinicians should maintain vigilance for pedicle torsion of subserosal fibroids in pregnant patients with large uterine fibroids, given the distinct physiological changes of pregnancy. The risk of pedicle torsion increases further after labor onset; severe torsion may result in uterine rupture, and diagnosis may be particularly challenging, necessitating a high level of clinical suspicion.

Uterine fibroid rupture results from the interplay of multiple factors, encompassing vascular abnormalities and hormonal regulation among other multidimensional mechanisms. Although most fibroids are asymptomatic, under certain conditions such as pregnancy, trauma, or rapid growth, they may rupture, leading to serious complications including intra-abdominal hemorrhage, infection, or even shock. During pregnancy, increased uterine blood flow and elevated internal pressure within the fibroid heighten the risk; when patients with concurrent pregnancy and uterine fibroids enter labor, uterine contractions or increased intra-abdominal pressure during vaginal delivery may both precipitate compression and rupture of the fibroid [16] . The high-estrogen and progesterone state characteristic of pregnancy promotes fibroid cell proliferation and inhibits collagen synthesis, thereby weakening tissue integrity and accelerating the rupture process. Furthermore, literature indicates that pedunculated subserosal uterine fibroids are more prone to torsion, which can induce ischemic necrosis and markedly increase the risk of rupture [17] . In this case, intraoperative findings during cesarean section revealed a 720˚ torsion of a subserosal uterine fibroid, where traction on the fibroid’s pedicle resulted in rupture and hemorrhage of the uterine myometrium. Although this patient experienced uterine rupture and bleeding due to fibroid torsion without fibroid rupture, this scenario nonetheless highlights for clinicians that in patients with pedunculated subserosal uterine fibroids, the risk of fibroid pedicle torsion increases after entering labor. Vigilance is warranted regarding the potential for fibroid rupture exacerbation induced by pedicle torsion; clinicians should conduct comprehensive risk assessment and develop individualized prevention and management strategies to enhance early clinical identification capability.

The incidence of premature rupture of membranes (PROM) is approximately 8% - 12%. According to studies, the risk of PROM is significantly higher in pregnant patients with uterine fibroids than in those without fibroids (6.8% vs 0.5%, P = 0.01). Furthermore, patients with large fibroids (diameter > 5 cm) exhibit a higher rate of PROM compared to those with small fibroids (diameter < 5 cm) [18] [19] . This increased risk may be attributed to elevated intrauterine pressure from larger or multiple fibroids, which promotes apoptosis of fetal membrane cells, enhances inflammatory activity, increases membrane fragility, and lowers the threshold for rupture, thereby inducing PROM [20] . In the current case, the patient, a primigravida, experienced sudden PROM at 37+ weeks of gestation. Although the patient was diagnosed with gestational diabetes during pregnancy and subsequently tested positive for nucleic acid in the reproductive tract after admission, the occurrence of PROM may be influenced by multiple factors. Nevertheless, this case highlights the importance for clinicians to remain vigilant for PROM and subsequent delivery in pregnant women with large uterine fibroids during prenatal examinations; this warning is particularly significant for those who are not yet at term. PROM is the most direct cause of preterm birth, with over 50% of PROM patients expected to deliver within one week [21] .