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. 2026 Aug 4;51:e00845. doi: 10.1016/j.crwh.2026.e00845

Delayed pyometra after uterine artery embolization for uterine leiomyoma: A case report

Seong Hee Jeon 1, Jo Hyun Kim 1, Seung Joo Chon 1,⁎
PMCID: PMC13474021  PMID: 42602499

Abstract

Uterine artery embolization is a minimally invasive, uterus-preserving treatment for symptomatic uterine leiomyomas that is generally considered safe; delayed infectious complications are uncommon and may be difficult to distinguish from postembolization syndrome.

This report presents a case of delayed pyometra associated with a necrotizing leiomyoma following uterine artery embolization. A 41-year-old multiparous woman with a history of two cesarean deliveries underwent bilateral uterine artery embolization for a symptomatic large FIGO type 2 submucosal leiomyoma after declining surgical treatment. Although her symptoms initially improved, she presented three months later with high fever and severe pelvic pain despite only mildly elevated inflammatory laboratory findings. Imaging demonstrated a necrotic leiomyoma with pyometra, and endometrial culture yielded Streptococcus agalactiae. Despite uterine drainage and culture-directed antimicrobial therapy, persistent symptoms ultimately required total laparoscopic hysterectomy. Histopathological examination confirmed extensive coagulative necrosis of the leiomyoma with acute inflammatory infiltration.

This case highlights that delayed infectious complications may occur several months after uterine artery embolization for large submucosal leiomyomas and may mimic postembolization syndrome despite relatively mild inflammatory laboratory abnormalities. Careful long-term follow-up and prompt evaluation are essential for timely diagnosis and appropriate management.

Keywords: Infection, Leiomyoma, Necrosis, Pyometra, Uterine artery embolization

Highlights

  • •

    In the reported case, pyometra developed three months after uterine artery embolization.

  • •

    Submucosal leiomyomas may increase the risk of secondary infection.

  • •

    Delayed infection may mimic postembolization syndrome.

  • •

    Persistent fever warrants prompt evaluation for delayed infection.

  • •

    Surgical management may be required when conservative treatment fails.

1. Introduction

Uterine artery embolization (UAE) has become an established minimally invasive, uterus-preserving treatment for symptomatic uterine leiomyomas [1], [2], [3], [4]. By occluding the uterine arteries, UAE induces ischemic degeneration of leiomyomas, resulting in symptom relief. Although generally considered safe, complications have been reported, including postembolization syndrome, leiomyoma expulsion, and uterine necrosis, as well as infectious complications such as endometritis, pyomyoma, and pyometra [2], [5], [6].

Postembolization syndrome typically presents with pelvic pain, fever, and inflammatory symptoms shortly after the procedure and is usually self-limited. In contrast, delayed infectious complications are uncommon but may progress to severe pelvic infection or sepsis if not promptly recognized [7]. Because delayed infection may clinically mimic postembolization syndrome early diagnosis can be challenging, but is important because the two conditions require substantially different management. Although several cases of pyomyoma and other severe infectious complications after UAE have been described [8], [9], delayed presentations occurring several months after embolization accompanied by only mild inflammatory laboratory abnormalities remain rarely reported.

This report concerns a case of delayed pyometra associated with a necrotizing FIGO type 2 submucosal leiomyoma that developed three months after UAE. It highlights the diagnostic challenge of distinguishing delayed infection from postembolization syndrome despite relatively mild inflammatory laboratory abnormalities and discusses the rationale for treatment selection and subsequent management.

2. Case Presentation

A 41-year-old multiparous woman with a history of two previous cesarean deliveries presented to a local clinic with heavy menstrual bleeding and progressive dysmenorrhea. Transvaginal ultrasonography revealed a submucosal uterine leiomyoma measuring approximately 7.8 cm. Pelvic magnetic resonance imaging (MRI) performed before treatment demonstrated an 8-cm FIGO type 2 submucosal leiomyoma distorting the endometrial cavity (Fig. 1) [10]. Myomectomy was initially recommended at another tertiary referral center because of the size and location of the leiomyoma. However, the patient wished to avoid surgery and preferred uterus-preserving, nonsurgical treatment. After counseling regarding treatment options, the patient elected to undergo bilateral UAE. No prophylactic antibiotics were administered at the time of embolization.

Fig. 1.

Fig. 1

Pre-procedural sagittal T2-weighted magnetic resonance image demonstrating an approximately 8-cm submucosal leiomyoma distorting the endometrial cavity.

Pelvic angiography performed before embolization demonstrated bilateral uterine artery enlargement with hypervascular staining of the leiomyoma (Fig. 2A, B). Embolization was performed using non-absorbable spherical embolic particles (EmboSphere; 500–700 μm, 4 cc; 700–900 μm, 14 cc). Post-embolization angiography confirmed successful occlusion of both uterine arteries with markedly reduced perfusion to the lesion (Fig. 2C, D).

Fig. 2.

Fig. 2

Pelvic angiography before and after uterine artery embolization. (A, B) Pelvic angiography before embolization demonstrating hypervascular staining of the leiomyoma. (C, D) Post-embolization angiography showing near-complete devascularization of the leiomyoma.

Three months after UAE, the patient developed persistent fever, lower abdominal pain, and worsening dysmenorrhea. She initially visited a local clinic, where uterine evacuation was considered but not performed because ultrasonography demonstrated the uterine leiomyoma without evidence of retained intrauterine contents. She subsequently returned to the tertiary referral center where UAE had been performed, and laparoscopic myomectomy was planned. Before the scheduled surgery, worsening symptoms prompted presentation to another emergency department.

On presentation, her temperature was 39 °C. She appeared ill but was hemodynamically stable, with diffuse lower abdominal tenderness without rebound tenderness. Laboratory findings showed hemoglobin 10.0 g/dL, white blood cell count 5.73 × 103/μL, absolute neutrophil count 4166/μL, and elevated C-reactive protein 1.58 mg/dL. Blood cultures were negative. Pelvic examination demonstrated purulent, blood‑tinged vaginal discharge with cervical motion tenderness. Contrast-enhanced computed tomography (CT) revealed a non-enhancing intrauterine mass suggestive of necrotic degeneration of the leiomyoma (Fig. 3A). MRI demonstrated a distended uterine cavity containing fluid consistent with pyometra and possible hematometra (Fig. 3B). These findings raised suspicion for a delayed infectious complication associated with a necrotizing leiomyoma following UAE.

Fig. 3.

Fig. 3

Imaging findings at clinical deterioration. (A) Sagittal contrast-enhanced CT scan showing intrauterine fluid collection suggestive of pyometra and possible hematometra. (B) Sagittal T2-weighted MRI scan demonstrating a heterogeneous submucosal mass with necrotic areas (low signal) and retained fluid (high signal).

Uterine drainage by dilatation and evacuation was attempted after admission; however, only a small amount of purulent material could be evacuated despite the marked intrauterine collection demonstrated on imaging. Following consultation with the infectious diseases department, empirical antimicrobial therapy with intravenous vancomycin, ceftriaxone, and oral doxycycline was initiated. Endometrial culture yielded Streptococcus agalactiae (Group B streptococcus), and antimicrobial therapy was subsequently de-escalated to intravenous ampicillin/sulbactam according to susceptibility testing. Despite uterine drainage and culture-directed antimicrobial therapy, the patient remained symptomatic even though inflammatory markers gradually improved.

Because conservative management failed to achieve adequate clinical improvement and the patient ultimately preferred definitive treatment after persistent symptoms and repeated medical visits, total laparoscopic hysterectomy was performed 116 days after UAE. Intraoperatively, the uterus was enlarged with a smooth external surface and no evidence of pelvic adhesions or gross purulent contamination. The procedure was completed without complications.

Histopathological examination demonstrated extensive coagulative necrosis of the leiomyoma with surrounding acute inflammatory cell infiltration (Fig. 4A, B). These findings are consistent with previously reported histopathological changes following UAE [11].

Fig. 4.

Fig. 4

Histopathological findings. (A) Coagulative necrosis of leiomyoma showing preserved muscle fibers without nuclei (H&E, ×400). (B) Embolization particles within a uterine vessel with surrounding foreign body reaction (H&E, ×200).

The postoperative course was uneventful. No additional antibiotic therapy was required, and she was discharged on postoperative day 2. At 6-month follow-up, she remained asymptomatic with no evidence of recurrent infection.

3. Discussion

In the present case, pyometra developed approximately three months after UAE for a large FIGO type 2 submucosal leiomyoma, representing an unusual delayed infectious complication. Although infectious complications following UAE are uncommon, they remain clinically important because they may progress to severe pelvic infection or sepsis if diagnosis and source control are delayed [7]. The most distinctive features of this case were the delayed presentation, relatively mild inflammatory laboratory abnormalities despite clinically significant infection, and failure of conservative management despite uterine drainage and culture-directed antimicrobial therapy.

The choice of initial treatment warrants careful consideration. Hysteroscopic resection is generally considered an appropriate uterus-preserving treatment for selected submucosal leiomyomas [12]. However, in the present case, the leiomyoma measured approximately 8 cm and was classified as FIGO type 2, making complete hysteroscopic resection technically challenging because of its large size and substantial intramural component. Myomectomy was initially recommended because of the size and location of the leiomyoma; however, the patient strongly desired not only uterine preservation but also avoidance of surgical treatment. After counseling regarding the potential risks and benefits of each treatment option, UAE was selected through shared decision-making as a minimally invasive, uterus-preserving alternative.

The mechanism of infection in this case is supported by both the anatomical characteristics of the leiomyoma and the pathological findings. Histopathological examination confirmed extensive coagulative necrosis following embolization. Unlike pedunculated submucosal leiomyomas, FIGO type 2 lesions retain a substantial intramural component while remaining in direct contact with the endometrial cavity. Following UAE, infarcted tissue may therefore become exposed to the uterine cavity, facilitating ascending bacterial colonization from the lower genital tract [13]. Furthermore, distortion of the endometrial cavity by the large submucosal leiomyoma may impair drainage of infected material, promoting the development of pyometra. Isolation of Streptococcus agalactiae, a common colonizer of the lower genital tract, supports this proposed mechanism [14].

Submucosal leiomyomas have been associated with higher risks of fibroid expulsion and secondary intrauterine infection after UAE because of their anatomical relationship with the endometrial cavity [13], [15], [16]. Despite this increased risk, submucosal location is not considered an absolute contraindication to UAE, and embolization remains an accepted uterus-preserving treatment option in carefully selected patients. In the present case, the large submucosal leiomyoma likely increased the risk of post-embolization necrosis and secondary infection. Rather than representing an unexpected complication occurring in the absence of risk factors, this case illustrates an unusually delayed presentation of a recognized complication after UAE.

Another important aspect of this case was the failure of conservative management despite appropriate source-control measures. Uterine drainage was attempted after admission; however, only a small amount of purulent material could be evacuated despite the large intrauterine collection demonstrated on imaging. One possible explanation is that communication between the necrotic leiomyoma and the uterine cavity remained incomplete because most of the lesion was still embedded within the myometrium. In addition, incomplete liquefaction of infarcted tissue may have limited adequate drainage. Although these mechanisms remain speculative, they are consistent with the marked discrepancy between the imaging findings and the limited amount of drainage obtained.

Persistent symptoms despite uterine drainage and culture-directed antimicrobial therapy suggested inadequate source control. Although further conservative management might theoretically have allowed additional liquefaction or spontaneous drainage of necrotic tissue, continued observation was considered inappropriate given the persistent symptoms and the risk of progression to severe pelvic infection or sepsis. After repeated medical visits and persistent symptoms, the patient ultimately elected to have definitive surgical treatment. Total laparoscopic hysterectomy successfully removed the infectious source, and the uneventful postoperative recovery without additional antibiotic therapy further supports that definitive source control was required in this case.

Another noteworthy feature was the delayed timing of presentation. Distinguishing delayed infectious complications from postembolization syndrome represents an important clinical challenge because the two conditions require fundamentally different management strategies (Table 1). Postembolization syndrome typically develops within the first few days after UAE and is characterized by self-limited fever and pelvic pain, whereas delayed infection usually presents weeks to months later with persistent or high-grade fever and progressive pelvic pain, and may require antibiotics or surgical intervention [2]. In contrast, this patient presented approximately three months after embolization with high fever and severe pelvic pain, while the white blood cell count remained within the normal range and C-reactive protein was only mildly elevated. Such a relatively inconspicuous laboratory response may delay diagnosis because delayed infection can clinically resemble postembolization syndrome or other benign post-procedural conditions. Therefore, delayed infection should remain in the differential diagnosis for patients presenting with persistent fever or pelvic pain after UAE, even when inflammatory laboratory abnormalities are modest.

Table 1.

Clinical differentiation between postembolization syndrome and delayed infectious complications after uterine artery embolization.

Feature Early post-embolization syndrome Delayed infectious complication
Onset Within a few days Weeks to months
Fever Low-grade Persistent or high-grade
Pain Mild to moderate, self-limited Progressive or severe
Vaginal discharge Usually absent May be present (often foul-smelling)
Treatment Supportive care (analgesics, NSAIDs) Antibiotics ± surgical intervention
Clinical implication Benign, self-limited Requires prompt evaluation and possibly intervention

This case demonstrates that delayed infectious complications may occur even after an initially uneventful recovery following UAE. These findings underscore the importance of careful preprocedural counseling for patients with large FIGO type 2 submucosal leiomyomas. Although UAE remains an appropriate uterus-preserving treatment option for carefully selected patients, continued clinical follow-up beyond the immediate post-procedural period is warranted. In patients presenting with persistent fever or pelvic pain after UAE, delayed infection should be considered even when inflammatory laboratory abnormalities are modest. Prompt imaging, microbiological evaluation, adequate drainage when feasible, and timely surgical source control are essential to prevent progression to severe pelvic infection or sepsis.

4. Conclusion

In conclusion, delayed pyometra should be considered in patients presenting with persistent fever or pelvic pain after uterine artery embolization, even when inflammatory laboratory abnormalities are modest. Early recognition and timely source control are essential to prevent progression to severe pelvic infection or sepsis.

Contributors

Seong Hee Jeon contributed to patient care, conception of the case report, acquiring the data, drafting the manuscript, undertaking the literature review and revising the article critically for important intellectual content.

Jo Hyun Kim contributed to acquiring the data and revising the article critically for important intellectual content.

Seung Joo Chon contributed to patient care, conception of the case report and revising the article critically for important intellectual content.

All authors approved the final submitted manuscript.

Patient consent

Written informed consent was obtained from the patient for publication of the case report and accompanying images.

Provenance and peer review

This article was not commissioned and was peer reviewed.

Funding

No funding from an external source supported the publication of this case report.

Declaration of competing interest

The authors declare that they have no competing interest regarding the publication of this case report.

References

  • 1.Ravina J.H., et al. Arterial embolisation to treat uterine myomata. Lancet. 1995;346(8976):671–672. doi: 10.1016/s0140-6736(95)92282-2. [DOI] [PubMed] [Google Scholar]
  • 2.Spies J.B., et al. Uterine artery embolization for leiomyomata. Obstet. Gynecol. 2001;98(1):29–34. doi: 10.1016/s0029-7844(01)01382-5. [DOI] [PubMed] [Google Scholar]
  • 3.Gupta J.K., et al. Uterine artery embolization for symptomatic uterine fibroids. Cochrane Database Syst. Rev. 2014;2014(12):CD005073. doi: 10.1002/14651858.CD005073.pub4. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.Goodwin S.C., et al. Uterine artery embolization for the treatment of uterine leiomyomata midterm results. J. Vasc. Interv. Radiol. 1999;10(9):1159–1165. doi: 10.1016/s1051-0443(99)70213-7. [DOI] [PubMed] [Google Scholar]
  • 5.Frenk N.E., et al. Predictors and clinical outcomes of fibroid expulsion after uterine artery embolization. Cardiovasc. Intervent. Radiol. 2023;46(11):1583–1593. doi: 10.1007/s00270-023-03532-9. [DOI] [PubMed] [Google Scholar]
  • 6.Torigian D.A., et al. MRI of uterine necrosis after uterine artery embolization for treatment of uterine leiomyomata. AJR Am. J. Roentgenol. 2005;184(2):555–559. doi: 10.2214/ajr.184.2.01840555. [DOI] [PubMed] [Google Scholar]
  • 7.de Blok S., et al. Fatal sepsis after uterine artery embolization with microspheres. J. Vasc. Interv. Radiol. 2003;14(6):779–783. doi: 10.1097/01.rvi.0000079988.80153.61. [DOI] [PubMed] [Google Scholar]
  • 8.Busshoff J., Thangarajah F., Morgenstern B. Uterus-preserving management of pyomyoma: case report of a rare complication after uterine artery embolization. Case Rep. Womens Health. 2022;34 doi: 10.1016/j.crwh.2022.e00405. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Ezzedine D., et al. Pyomyoma after uterine artery embolization: a case report. Case Rep. Womens Health. 2020;26 doi: 10.1016/j.crwh.2020.e00186. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10.Lakabi R., et al. Diagnosis and classification of uterine fibroids. Int. J. Gynaecol. Obstet. 2025;171(2):566–573. doi: 10.1002/ijgo.70538. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 11.McCluggage W.G., et al. Pathologic features of uterine leiomyomas following uterine artery embolization. Int. J. Gynecol. Pathol. 2000;19(4):342–347. doi: 10.1097/00004347-200010000-00008. [DOI] [PubMed] [Google Scholar]
  • 12.Clark T.J., et al. European Society for gynaecological endoscopy (ESGE) good practice recommendations on surgical techniques for removal of fibroids: part 2 hysteroscopic myomectomy. Facts Views Vis. Obgyn. 2024;16(4):383–397. doi: 10.52054/FVVO.16.4.054. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13.Lukies M., Clements W. Current strategies for prevention of infection after uterine artery embolisation. Cardiovasc. Intervent. Radiol. 2022;45(7):911–917. doi: 10.1007/s00270-022-03158-3. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14.Armistead B., et al. The double life of Group B Streptococcus: asymptomatic colonizer and potent pathogen. J. Mol. Biol. 2019;431(16):2914–2931. doi: 10.1016/j.jmb.2019.01.035. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15.Rajan D.K., et al. Risk of intrauterine infectious complications after uterine artery embolization. J. Vasc. Interv. Radiol. 2004;15(12):1415–1421. doi: 10.1097/01.RVI.0000141337.52684.C4. [DOI] [PubMed] [Google Scholar]
  • 16.Schirf B.E., Vogelzang R.L., Chrisman H.B. Complications of uterine fibroid embolization. Semin. Intervent. Radiol. 2006;23(2):143–149. doi: 10.1055/s-2006-941444. [DOI] [PMC free article] [PubMed] [Google Scholar]

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