Our retrospective cohort of 651 fibroid-affected pregnancies is one of the largest single-center studies to evaluate obstetric outcomes by fibroid size. The major finding is a clear size-dependent impact of uterine fibroids on pregnancy course and outcome. Women harboring large fibroids (> 10 cm) had substantially higher risks of adverse outcomes notably preterm birth, malpresentation, cesarean delivery, and PPH compared to those with smaller fibroids. In our cohort, nearly one in three women with fibroids > 10 cm delivered before 37 weeks’ gestation, and almost half had a non-cephalic fetal presentation at term (compared to 13.3% with fibroids < 5 cm). The caesarean section rate rose to 92.1% in the > 10 cm group versus 56.6% in the < 5 cm group, reflecting both elective pre-labor decisions and intrapartum complications. Perhaps most striking, PPH occurred in nearly one-third of women with > 10 cm fibroids, a marked increase over those with small fibroids. Neonatal outcomes were also impacted: larger fibroids were associated with lower median birthweight, more neonatal intensive care unit admissions, and higher rates of respiratory complications in the newborn. In contrast, we observed that small fibroids (< 5 cm) – which comprised the majority of cases – were not associated with significant increases in adverse outcomes. These findings underscore the clinical significance of fibroid burden in pregnancy: fibroid size emerges as a key determinant of risk, and pregnancies complicated by large fibroids should be recognized as high-risk and managed accordingly.
Large or strategically situated uterine fibroids trigger a cascade of interconnected pathophysiological processes that plausibly explain the spectrum of complications we and others have observed. Mechanically, bulky intramural, cervical or lower-segment myomas distort the uterine cavity, limiting fetal rotation and descent, which increases breech or transverse lie and, consequently, caesarean delivery; submucosal nodules that protrude into the endometrial cavity further reduce space for implantation, heightening miscarriage risk and early pregnancy bleeding as well as provoking abnormal placentation and regional uteroplacental hypoperfusion that can manifest clinically as fetal growth restriction [9]. Hypervascular fibroid tissue “steals” blood flow from surrounding myometrium, while very large lesions may outgrow their own supply and undergo red degeneration events that incite local inflammation, uterine irritability, cervical shortening and ultimately preterm labour [10, 11]. Distortion-induced over-distension or focal necrosis of the decidua can also weaken membranes, offering a biologically plausible route to the higher rates of PPROM in women with large fibroids [9]. Equally important is myometrial dysfunction: fibroid-laden muscle is less compliant and less responsive to oxytocin, so during labour it predisposes to dystocia and, in the third stage, to uterine atony a principal driver of PPH [12]. These synergistic effects; geometric distortion, vascular competition, inflammatory degeneration and impaired contractility constitute a coherent pathophysiological mosaic that explains why increasing fibroid diameter in our cohort was accompanied by stepwise rises in malpresentation, preterm delivery, PPROM and PPH [13].
Our results are broadly consistent with recent international studies. Prior large-scale analyses have likewise found that pregnant women with fibroids face elevated obstetric risks. A multicenter study from China by Zhao et al. involving approximately 112,000 births reported that the presence of uterine fibroids independently increased the odds of breech presentation (adjusted OR = 1.3), cesarean delivery (OR = 1.8), and postpartum hemorrhage (OR = 1.2). Importantly, that study noted the effect of fibroid size: PPH rates rose significantly as fibroid diameter increased, mirroring our finding of a three-fold jump in PPH from the smallest to the largest fibroid group [14]. Additionally, Zhao et al. observed fibroid location matters, with intramural fibroids conferring the highest PPH risk (8.6% vs. 5% with submucosal or subserosal). Our cohort similarly suggests that deeply embedded fibroids (often intramural) carry greater hemorrhage risk, likely due to impaired uterine contractility post-delivery. A seven-hospital study by Krewson et al. corroborated these findings: compared with women whose fibroids measured < 5 cm, those with medium-sized fibroids (5–10 cm) and large fibroids (> 10 cm) had 1.7-fold and 2.4-fold higher odds, respectively, of severe postpartum hemorrhage requiring transfusion. Notably, that study found fibroid number was not an independent predictor of hemorrhage risk, consistent with our observation that having multiple fibroids did not significantly worsen outcomes beyond what was attributable to overall fibroid bulk [15]. Together, these data reinforce that it is the size and location of fibroids – rather than sheer quantity – that drive most adverse outcomes, a point of practical significance for risk stratification.
Fibroid-associated preterm birth has been a consistent finding across studies. A recent systematic review and meta-analysis (18 studies, > 276,000 pregnancies) confirmed that women with fibroids have higher odds of delivering preterm (RR = 1.4 for < 37 weeks) and that this relative risk increases for earlier gestational ages (e.g. RR > 2 for extreme prematurity < 28 weeks) [16]. Our data align with this trend – the rate of < 37 week delivery doubled from 12 to 24% with fibroids 5–10 cm, and tripled (36%) with fibroids > 10 cm. Karlsen et al., in their Danish nationwide cohort of 92,696 pregnancies, reported that uterine fibroids were associated with a 2.3-fold increase in overall preterm birth and an even higher risk of extreme preterm delivery [17]. Those authors also noted an increased likelihood of elective cesarean delivery in women with fibroids (consistent with our finding of many fibroid patients delivering by planned C-section). The fibroid–CS association is well-documented; fibroids can increase the overall cesarean risk by roughly 1.5–2-fold, often due to malpresentation or labor dystocia. Indeed, malpresentation is a recurrent theme: research from both East and West has found fibroids predispose to non-vertex presentation [14]. Our study’s nearly 50% malpresentation rate in the > 10 cm group is in line with these reports and emphasizes how large fibroids distort uterine anatomy, preventing fetal head engagement.
One of the most debated topics has been fibroids’ influence on miscarriage. Submucosal fibroids have long been thought to raise miscarriage risk via cavity distortion [18]. However, recent evidence has challenged the extent of this effect. A notable prospective cohort study by Hartmann et al. found that, when controlling for confounders like age and race, women with fibroids had an identical first-trimester miscarriage rate (11%) as women without fibroids [19]. In our cohort, we observed miscarriage rates (14.5%) in fibroid patients that were within expected population ranges, and no clear size-dependent increase in first-trimester loss. It is possible that only certain fibroid types (especially submucosal myomas that deform the endometrial cavity) truly impact early pregnancy viability. Indeed, consensus reviews note that submucous fibroids have the greatest negative impact on fertility and miscarriage, whereas purely intramural or subserosal fibroids have a less clear or minimal effect on early pregnancy maintenance [20].
Few large studies reported detailed neonatal morbidity, but available data indicate some impact of fibroids on neonatal health, largely secondary to prematurity. In Choudhary et al.’s cohort, one in five infants required NICU care [1]. Another retrospective study by Ranjan et al. documented NICU admission in 15% of fibroid-affected pregnancies and low 5-minute Apgar scores (< 7) in 8% [21]. These figures are in line with the higher neonatal risks we observed in our fibroid group. Increased NICU admissions are likely driven by the greater incidence of preterm births and possibly growth restriction or distress at birth. Indeed, fetal growth issues have been noted in some studies – for example, the Right from the Start cohort found a significant birthweight reduction when multiple fibroids were present [22]. Krewson et al. have also reported higher rates of low birth weight and fetal distress in fibroid pregnancies [23]. Although direct associations with neonatal respiratory distress syndrome or sepsis have not been prominent in the literature, the increased preterm delivery and PPROM rates in fibroid pregnancies suggest that neonates born to mothers with fibroids may face higher risks of complications related to prematurity (respiratory difficulties, neonatal infection, etc.). This aligns with the trend of more frequent NICU stays and resuscitations required in these cohorts.
Previous international reports have yielded modest but non-trivial elevations in placenta-centered morbidity among women with fibroids. In the 24-study meta-analysis by Li et al., the pooled placenta previa rate was 2.48% in fibroid pregnancies versus 0.98% in controls—a nearly three-fold excess risk (RR = 2.99, 95% CI 2.06–4.35) [8]. Likewise, the systematic review by Wang et al. reported a 60% increase in placental abruption (OR 1.60, 95% CI 1.20–2.14) among fibroid carriers [4]. By contrast, the large Chinese multicentre cohort of Zhao et al. found only a small, non-significant difference in previa incidence 1.9% with fibroids vs. 1.2% without (adjusted OR = 1.1, p = 0.17) and no rise in abruption (1.8% vs. 1.7%) [14]. Our study aligns with the latter observation: despite robust size-stratified effects for preterm birth, malpresentation and PPH, we detected no significant increase in either placenta previa (< 5%) or abruption (< 2%) across any fibroid-size group. Several explanations are plausible. First, both outcomes are rare; even in a cohort of 651 pregnancies the absolute event counts were low, limiting statistical power to detect modest risk increments. Second, the overwhelming majority of our leiomyomas were corporally intramural; prior data suggest that heightened previa/abruption risk is driven chiefly by lower-segment or submucosal lesions that physically overlap the placental implantation zone a pattern uncommon in our series [24]. These considerations imply that placenta fibroid spatial relationship and location may be more critical than size alone in determining previa or abruption risk. Prospective, multicentre studies using three-dimensional ultrasound or MRI to quantify placenta–fibroid distance are needed to clarify when targeted monitoring for placenta-related complications is warranted.
In our cohort, FGR displayed a clear size-gradient rising from ≈ 4% in pregnancies with fibroids < 5 cm to 16.7% when the dominant lesion exceeded 10 cm. This pattern is biologically plausible: large intramural masses may compete for uteroplacental perfusion and mechanically compress the placental bed, thereby curtailing fetal growth. International data are mixed but broadly support a size- or burden-dependent effect. The 24-study meta-analysis by Li et al. reported that fibroids increased the odds of low-birth-weight infants by ~ 30% and identified lesions ≥ 5 cm as the principal driver of that excess risk [8]. Conversely, a cohort analysed by Karlsen et al. 2020 which grouped all fibroid types and sizes together found no significant association with FGR after multivariable adjustment, suggesting that size-specific effects can be diluted when fibroids are treated as a single category [17]. Evidence from the prospective, community-based Right from the Start study strengthens this view. Edwards et al. observed no overall birth-weight decrement in women with fibroids, but a ≈ 200 g reduction when ≥ 3 fibroids were present, indicating that greater tumour burden by size or number matters most [22]. A more recent systematic review by Wang et al. likewise documented a modest yet significant mean birth-weight decrease of ≈ 118 g in fibroid-affected pregnancies [4]. Taken together, these data place our findings at the upper end of the reported risk spectrum and reinforce the concept that large or multiple leiomyomas, rather than fibroid presence per se, are the key determinants of impaired fetal growth. Future studies that quantify fibroid–placenta proximity with three-dimensional ultrasound or MRI could better delineate the threshold at which vascular competition translates into clinically relevant FGR.
Broad evidence syntheses affirm that fibroids modestly increase the risk of various adverse outcomes. A recent comprehensive meta-analysis by Li et al. confirmed that pregnancies with fibroids have higher odds of preterm birth, cesarean delivery, placental complications, PROM/PPROM, PPH, and neonatal complications such as low birth weight [8]. For example, fibroid presence was associated with a 1.7-fold risk of preterm birth and 1.9-fold risk of CS, as well as nearly triple the risk of placenta previa and 3.5-fold risk of PPH in pooled data. Importantly, this meta-analysis performed subgroup analyses by fibroid size and found that large fibroids conferred significantly greater risk than small fibroids for certain outcomes [23]. In women with large fibroids (generally ≥ 5 cm), the risk of breech presentation was 1.5 times higher, placenta previa ~ 5 times higher, and PPH 1.6 times higher compared to those with only small fibroids. These findings closely mirror the size-stratified patterns in our study, lending weight to our observation that fibroid size is a key determinant of obstetric risk. In contrast, the influence of fibroid location is less consistently reported across studies – while Zhao et al. highlighted intramural fibroids as particularly deleterious for PPH, other cohorts did not observe location-based differences [1, 12, 22]. Taken together, however, the literature supports that multiple or large fibroids are especially likely to worsen pregnancy outcomes, which aligns with the elevated complications we found in cases of higher fibroid burden.
Our findings underscore the necessity of individualized antenatal care pathways in pregnancies complicated by fibroids exceeding 5 cm in diameter. For such patients, intensified surveillance during the third trimester—including serial sonographic assessments of fetal growth and fibroid morphology—should be considered standard practice. In cases involving fibroids > 10 cm, multidisciplinary delivery planning is advised, ideally within tertiary care centers equipped with immediate access to blood products and anesthesia teams experienced in managing complex obstetric hemorrhage. Elective delivery, typically via cesarean section between 37 and 38 weeks, may be warranted depending on fibroid location, distortion of uterine architecture, and obstetric history. Integration of these findings into clinical protocols may facilitate earlier identification of high-risk scenarios and improve maternal–fetal outcomes.
This study’s chief strengths are its systematic first-trimester ultrasonography—which captured both asymptomatic leiomyomas and early-pregnancy losses—its large sample size, and the uniform institutional protocol used to record detailed intra-operative metrics and neonatal endpoints. Stratifying tumours into < 5 cm, 5–10 cm and > 10 cm categories allowed us to demonstrate a clear, dose-responsive escalation of risk that “any-fibroid” studies often overlook, while the single-centre setting minimised measurement heterogeneity.
This study has several limitations. First, fibroid number, type, and location were recorded but not incorporated into the multivariate models, limiting our ability to assess their independent contribution to outcomes. Second, the absence of an internal fibroid-free control group necessitated reliance on external population data for baseline risk comparisons, which may introduce bias due to differing study populations. Third, rare events such as placenta previa and abruption yielded low case numbers, restricting statistical power to detect meaningful associations. Finally, the lack of serial imaging during pregnancy prevented evaluation of interval growth or degeneration, which may influence clinical course.
Several limitations warrant acknowledgement. The retrospective, tertiary-referral design may have introduced selection bias and limits external validity; an internal fibroid-free control arm was unavailable, so absolute risk differences were derived from external benchmarks. Rare outcomes such as placenta previa and abruption generated few events, restricting statistical power, and the absence of serial imaging meant interval growth or degeneration—potential modifiers of risk—could not be assessed. Future work should include prospective, multicentre cohorts that use 3-D ultrasound or MRI to quantify fibroid–placenta proximity, as well as randomised or rigorously matched studies evaluating pre-pregnancy myomectomy and emerging minimally invasive therapies (e.g., focused ultrasound). Long-term neonatal follow-up will also be essential to determine whether fibroid-related prematurity confers lasting health or developmental burdens.Formun Altı.