Discussion

Uterine fibroids, or leiomyomas, are the most common benign uterine neoplasm in women and are primarily composed of smooth muscle and fibrous connective tissue. Leiomyomas can be classified as submucosal, intramural, or subserosal depending on location.¹ Most leiomyomas are asymptomatic but may present with abnormal uterine bleeding, pain from pressure on abdominal organs, or a palpable abdominal mass.¹ Although benign, there are several complications of fibroids that may necessitate intervention. Intra-abdominal hemorrhage due to a ruptured uterine fibroid is extremely rare. Only 125 cases were identified in a 2020 systematic review of the literature for the past century.² An intraperitoneal hemorrhage from a fibroid is typically secondary to rupture of superficial veins due to an increase in abdominal pressure.³ The resulting bleeding can less frequently be arterial in nature or related to hypertension.³ Other etiologies for intra-abdominal hemorrhage from a fibroid include avulsion due to trauma, torsion of a pedunculated fibroid, and vessel rupture due to venous congestion in menstruation, pregnancy, or strenuous exercise.^{3, 4}

The spontaneous rupture of a fibroid is exceedingly rare, with only ten cases reported in the last half-decade.³ Cases of spontaneous perforation most commonly involve a pathologic provoking factor, such as necrosis or infection, as in our case. Other possible provoking factors include post-dilation and curettage and increased intra-abdominal pressure.⁵ The bisected gross uterine specimen in our case exhibited uterine fibroids with areas of degeneration and necrosis. Microscopic examination of the surgical specimen from our patient demonstrated hyaline degeneration and ischemic necrosis of the leiomyoma. Hyaline degeneration occurs when smooth muscle is replaced by fibrous connective tissue, resulting in decreased stromal support and tissue integrity.⁵ This compromised tissue integrity, along with the noted necrotic tissue, could have precipitated a rupture from within the mass. The pathogenesis resulting in the degeneration of fibroids is multifactorial. An enlarging leiomyoma may outgrow its blood supply, resulting in several types of degeneration, including hyaline, calcified, cystic, and red.¹ The pathogenesis may also involve steroid hormones.³ Fibroids are responsive to estrogen and progesterone, with symptomatic fibroids being most common in perimenopausal women aged 40 or older.⁶ Menstrual cyclicity is another important factor affecting the maintenance and growth of fibroids.³ As our patient was perimenopausal, the pathological changes seen in her fibroid might have been related to decreasing levels of estrogen and progesterone and associated with menstrual cycle irregularity. These hormonal changes could have affected the vascular blood supply to her large fibroid, leading to degeneration and necrosis.

US, CT scans, and MRI have been used for the evaluation of ruptured leiomyomas.³ In our case, the CT scan was sufficient to identify the etiology of the small-volume hemoperitoneum, given the absence of the necrotic fibroid visualized on the previous CT. Pelvic US is safe and readily accessible, but the acuity of presentation led to prioritizing CT for a more derivative diagnosis in this scenario. One limitation of the US is the inability to assess for active bleeding and limitations in evaluating adjacent structures. CT angiography was performed to exclude active bleeding in our patient due to the presence of complex ascites. MRI can further delineate the nature of the diagnosis, but it is not appropriate in emergent cases due to acquisition time.⁴ Only 2 of the 125 patients identified by Lim et al. had an MRI performed.²