Spontaneous Expulsion of a Large Submucosal Fibroid in the Postpartum Period: A Report of a Rare Case

A 39-year-old pregnant lady with three previous vaginal deliveries was diagnosed with a large uterine fibroid during her fourth pregnancy. Early pregnancy ultrasound at six weeks' gestation demonstrated a large uterine fibroid measuring approximately 102.8 × 102.4 × 102.5 mm (Figure 1 ). Subsequent antenatal imaging showed an interval increase in fibroid size, measuring 139 × 118 × 152 mm at 16 weeks’ gestation, located in the left anterior uterine wall. Anomaly scan imaging again demonstrated a large fibroid, measuring approximately 142.2 × 124.3 mm (Figure 2 ). No additional uterine pathology was identified. The remainder of the pregnancy was uncomplicated, with no antenatal pain, bleeding, or preterm labour. She underwent an elective lower-segment caesarean section at term for persistent breech presentation. Intraoperatively, a large anterior uterine fibroid was visualised and left in situ. The procedure was complicated by an estimated blood loss of 1.1 litres, although the patient remained haemodynamically stable and did not require blood transfusion. Following delivery, the patient reported persistent heavy menstrual bleeding that significantly affected her quality of life. For this reason, oral progestogen was prescribed in primary care as initial medical management. This was ineffective, and she presented to the gynaecology emergency clinic at 12 weeks postnatally for further assessment. Secondary postpartum haemorrhage and retained products of conception were considered as part of the differential diagnosis. Abdominal examination revealed a uterus enlarged to approximately 26-week gestational size. Subsequent transabdominal ultrasound demonstrated a large submucosal fibroid measuring 116.5 × 92.5 × 100.7 mm, with significant distortion of the endometrial cavity. No clear sonographic evidence of retained products of conception was identified (Figure 3 ). No clear sonographic evidence of retained products of conception was identified, and the endometrial stripe could not be reliably measured due to cavity distortion by the fibroid. After comprehensive counselling regarding the available management options, including definitive surgical treatment with myomectomy or hysterectomy, the patient was planned for surgical management. In view of the large fibroid size, persistent bleeding symptoms, and anticipated operative complexity, GnRH agonist therapy was commenced as a preoperative temporising measure to reduce bleeding, improve symptoms, and potentially reduce fibroid vascularity and size before surgery. She received leuprorelin acetate 11.25 mg, planned as two doses administered three months apart. Following the first dose, she reported a marked improvement in menstrual bleeding and a reduction in pelvic pressure symptoms. Unexpectedly, approximately two months after the initial leuprorelin injection and before the second dose or planned surgical intervention, she spontaneously passed a large tissue mass per vagina. This was not associated with significant pain, haemorrhage, or infection. Histopathological examination demonstrated an entirely infarcted spindle cell lesion with ghost outlines of spindle cells. Although extensive infarction limited definitive assessment, the appearances were considered most in keeping with an infarcted smooth muscle tumour, consistent with an infarcted leiomyoma in the clinical context. Given the subsequent residual fibroid tissue seen on imaging, this was interpreted as spontaneous expulsion of the predominantly intracavitary component, followed by regression and calcification of the residual intramural component (Table 1 ). The table summarises the macroscopic and microscopic findings of the tissue mass passed vaginally. The findings were most consistent with an infarcted smooth muscle tumour, consistent with an infarcted leiomyoma in the clinical context. A follow-up ultrasound performed one month after spontaneous expulsion demonstrated marked interval reduction in fibroid size, with a residual anterior submucosal fibroid measuring approximately 30 × 24 × 34 mm (Figure 4 ). The case was discussed at a multidisciplinary team meeting, and interval reassessment with repeat imaging and diagnostic hysteroscopy was recommended to evaluate for residual disease and assess endometrial cavity integrity. Follow-up ultrasound performed one month after spontaneous vaginal expulsion of the fibroid, demonstrating marked interval reduction in size, with a residual anterior fibroid adjacent to the endometrial cavity measuring approximately 30 × 24 × 34 mm. A subsequent ultrasound performed three months later demonstrated a small calcified intramural fibroid measuring approximately 22 × 21 mm, located adjacent to the endometrial cavity, with a clearly defined endometrial thickness of 5.7 mm. Overall, the interval ultrasound findings demonstrated marked reduction in fibroid size following spontaneous expulsion, with subsequent calcification of the small residual intramural component adjacent to the endometrial cavity (Figure 5 ). Subsequent follow-up transvaginal ultrasound performed three months after the previous scan, demonstrating a small calcified intramural fibroid measuring approximately 22 × 21 mm adjacent to the endometrial cavity. Diagnostic hysteroscopy performed later that month revealed a normal uterine cavity, with no residual intracavitary fibroid or intrauterine adhesions. Follow-up endometrial biopsy demonstrated inactive endometrium, with no evidence of chronic endometritis, hyperplasia, or malignancy (Table 2 ). As the patient remained asymptomatic and all follow-up investigations were reassuring, she was discharged from gynaecology follow-up. This table summarises the histopathological findings of the spontaneously expelled tissue mass and subsequent follow-up endometrial biopsy. The expelled tissue showed extensive infarction, limiting definitive assessment, but the appearances were most in keeping with an infarcted smooth muscle tumour in the clinical context. Follow-up endometrial biopsy was reassuring, with no evidence of chronic endometritis, hyperplasia, or malignancy. A comparison with previously published cases of postpartum fibroid expulsion or regression and fibroid expulsion associated with GnRH therapy is summarised in Table 3 . This table summarises the chronological clinical course from antenatal diagnosis through postpartum symptoms, preoperative GnRH agonist therapy, spontaneous expulsion of the predominantly intracavitary component, and subsequent imaging, hysteroscopic and histological follow-up. GnRH: gonadotropin-releasing hormone

Uterine fibroids (leiomyomas) are the most common benign tumours of the female reproductive tract, with a cumulative incidence of up to 60% by the age of 35 years and over 80% by 50 years in some populations [ 1 , 2 ]. Although many fibroids are asymptomatic, their clinical presentation depends largely on size, number and anatomical location. Submucosal fibroids, which distort the endometrial cavity, are particularly associated with heavy menstrual bleeding, anaemia, subfertility and adverse reproductive outcomes, and are therefore more likely to require intervention [ 3 , 4 ]. Management options for uterine fibroids include expectant, medical and surgical approaches, tailored to symptom severity, reproductive wishes and patient preference [ 4 , 5 ]. Surgical treatment, including myomectomy or hysterectomy, remains definitive but is associated with operative risks and potential impact on fertility. Consequently, medical therapies such as gonadotropin-releasing hormone (GnRH) agonists are frequently used to reduce fibroid size and control symptoms, either as a temporising measure or as an adjunct to surgery [ 6 - 10 ]. Spontaneous expulsion of uterine fibroids is an uncommon clinical phenomenon. It has most frequently been reported in association with the postpartum period or following uterine artery embolisation, where uterine involution, altered vascular supply and increased myometrial contractility may contribute to fibroid degeneration and detachment [ 11 - 15 ]. In contrast, spontaneous expulsion in the absence of direct procedural intervention is rare, particularly for large fibroids. Although a small number of case reports have described fibroid expulsion during GnRH agonist therapy, these cases are uncommon and typically involve smaller or pedunculated lesions, and the causal relationship remains uncertain [ 16 - 19 ]. The interplay between postpartum physiological changes and medical therapy in facilitating fibroid expulsion is not well understood. We report a rare case of spontaneous expulsion of a very large submucosal fibroid in the postpartum period, with possible contribution from GnRH agonist therapy, resulting in complete resolution without surgical intervention.

Spontaneous expulsion of uterine fibroids is a rare but recognised clinical occurrence. It has most commonly been described in the postpartum period and following uterine artery embolisation, where physiological and vascular changes contribute to fibroid degeneration, detachment and eventual expulsion [ 12 - 15 ]. In contrast, expulsion occurring in the absence of direct procedural intervention remains uncommon, particularly for large fibroids. The postpartum period represents a unique physiological state in which uterine involution, reduced uterine blood flow and increased myometrial contractility may significantly influence fibroid behaviour. These changes can result in ischaemia, degeneration and, in some cases, migration of fibroids toward the endometrial cavity. Some case reports have described spontaneous regression or expulsion of fibroids following delivery, supporting the role of postpartum uterine remodelling as a key contributing mechanism [ 11 - 15 ]. In the present case, the fibroid, initially intramural during pregnancy, evolved into a predominantly submucosal lesion postpartum, suggesting dynamic structural changes that may have facilitated its eventual expulsion. Based on its postpartum relationship to the endometrial cavity, the lesion was considered most consistent with a submucosal fibroid, likely International Federation of Gynaecology and Obstetrics (FIGO) type 1-2. However, precise FIGO classification was limited by marked distortion of the endometrial cavity and the absence of MRI assessment. From an imaging perspective, the differential diagnosis for postpartum heavy menstrual bleeding with an enlarged uterus includes retained products of conception, postpartum haematoma, adenomyosis, degenerating fibroid, and, rarely, malignant uterine pathology. Retained products of conception were considered clinically; however, ultrasound demonstrated a well-defined large fibroid mass with marked distortion of the endometrial cavity and no clear intracavitary echogenic or vascular tissue suggestive of retained products. Postpartum haematoma was considered less likely given the chronic clinical course and serial imaging appearance. Adenomyosis was not supported by the presence of a dominant circumscribed mass lesion. Although sarcomatous change cannot be excluded by ultrasound alone, the subsequent spontaneous expulsion, histopathological findings most in keeping with an infarcted smooth muscle tumour, normal hysteroscopic cavity assessment, reassuring endometrial biopsy, clinical improvement, and endometrial cavity clearance supported a benign process. Although GnRH agonists are well established in reducing fibroid size and improving symptoms [ 6 - 10 ], their role in fibroid expulsion remains less clearly defined. GnRH agonists induce a hypo-oestrogenic state that reduces fibroid vascularity and promotes cellular apoptosis, potentially leading to ischaemic degeneration [ 6 - 10 ]. In submucosal or predominantly intracavitary fibroid components, such changes may weaken the attachment between the fibroid and the underlying myometrium, thereby facilitating separation. A limited number of case reports have described fibroid expulsion during GnRH agonist therapy; however, these typically involve smaller or pedunculated lesions [ 16 - 19 ]. Postpartum uterine involution, reduced uterine blood flow, fibroid infarction, and myometrial contractility were likely the predominant mechanisms in this case. This is supported by the recognised occurrence of fibroid expulsion in the postpartum period and after uterine artery embolisation, where vascular occlusion and subsequent ischaemic degeneration are central mechanisms. The temporal association with leuprorelin acetate is noteworthy; however, causality cannot be established from a single case. Leuprorelin may have reduced fibroid vascularity and promoted degeneration, but it cannot be determined whether expulsion would have occurred without GnRH agonist therapy. The exceptionally large size of the fibroid in this case- exceeding 11 cm - makes spontaneous expulsion particularly unusual. Most reported cases involve significantly smaller lesions, and large fibroids are generally managed surgically due to concerns regarding persistent symptoms, complications, and incomplete resolution [ 3 , 5 ]. In the present case, definitive surgical treatment was initially planned because of the fibroid size, persistent bleeding symptoms, and significant distortion of the endometrial cavity. GnRH agonist therapy was used as a preoperative temporising measure rather than as definitive conservative treatment. The subsequent spontaneous expulsion was therefore unexpected and altered the clinical course, allowing surgery to be avoided after reassuring post-expulsion assessment. A comparison with previously published cases of postpartum fibroid expulsion or regression and fibroid expulsion associated with GnRH therapy is summarised in Table 4 . This table summarises selected previously reported cases of spontaneous fibroid expulsion or regression in the postpartum period and cases associated with GnRH therapy. Compared with earlier reports, the present case is notable for the very large postpartum fibroid size, planned surgical management with leuprorelin acetate used as preoperative temporising therapy, unexpected spontaneous vaginal expulsion before planned surgery, and comprehensive follow-up with serial ultrasound, histopathology, hysteroscopy, and endometrial biopsy. GnRH: gonadotropin-releasing hormone Compared with previously reported cases, the present case is notable for the very large postpartum fibroid size, planned surgical management with preoperative GnRH agonist therapy, unexpected spontaneous vaginal expulsion before surgery, and comprehensive follow-up with serial ultrasound, histopathology, hysteroscopy, and endometrial biopsy. Importantly, spontaneous fibroid expulsion may be associated with complications including acute pain, heavy bleeding or infection, and clinicians should remain vigilant. Comprehensive post-expulsion evaluation is essential to confirm complete resolution and exclude retained tissue, intrauterine adhesions or endometrial pathology. In this case, serial imaging and diagnostic hysteroscopy confirmed complete clearance of the uterine cavity and restoration of normal endometrial architecture. Overall, this case supports the concept that spontaneous expulsion of submucosal fibroids, although rare, can occur as a result of multifactorial processes, particularly in the postpartum setting [ 11 - 15 ]. Medical therapy may act as an adjunctive factor rather than a primary cause [ 16 , 18 , 19 ]. Recognition of this possibility may help inform counselling and management decisions in selected patients seeking to avoid surgical intervention.

Spontaneous expulsion of a large submucosal fibroid is a rare but recognised clinical event, particularly in the postpartum setting. This case demonstrates spontaneous expulsion of the predominantly intracavitary component of a very large postpartum submucosal fibroid, temporally associated with preoperative GnRH agonist therapy. The subsequent clinical course showed marked regression and calcification of a small residual intramural component, with complete clearance of the endometrial cavity confirmed by hysteroscopy. Postpartum uterine involution, altered vascular dynamics, fibroid infarction, and myometrial contractility were likely important contributing factors, while leuprorelin acetate may have facilitated degeneration and expulsion. As causality cannot be established from a single case, the findings should be interpreted cautiously. Careful clinical, imaging, hysteroscopic, and histological follow-up is essential to confirm endometrial cavity clearance, exclude residual intracavitary or atypical pathology, and identify potential complications.