Uterine myomas occur in approximately 25% of reproductive-aged women and are noted on pathologic examination in approximately 80% of surgically excised uteri.1,2 The subset of parasitic myomas is rare, with few reported cases in the literature. Although first described by Kelly and Cullen in 1909, as “myomata that have for some reason become partially or almost completely separated from the uterus and receive their main blood-supply from another source,” the cause, natural history, and pathologic basis of parasitic myomas are still not clearly understood.3
The conventional thinking is that parasitic myomas are a rare variant of pedunculated subserosal myomas.4 It has been suggested that if a pedunculated subserosal myoma develops a long stalk and becomes what is termed a “wandering or migrating leiyomyoma”5 such a tumor can then go on to adhere to surrounding structures such as the omentum or broad ligament and develop an auxiliary blood supply. In this way, a “parasitic myoma” is formed when a “wandering myoma” loses its uterine blood supply and becomes attached and fed from a nonuterine source.
The literature has been limited to case reports and small series of such findings since the early 1900s3,4; more recently, a few case studies have identified parasitic myomas after laparoscopic morcellation procedures.6–10 Diagnosis of parasitic myomas is often incidental at the time of abdominal surgery for treatment of symptoms due to uterine myomas; however, there are case reports in which parasitic myomas have been found to cause symptoms themselves.6,9,11 We report our single institution experience with a series of 12 cases of parasitic myomas that were identified in a registry of surgical cases from August 2000 to April 2008.
MATERIALS AND METHODS
This is a retrospective review of 12 cases of parasitic myomas managed from 1992–2008 in a single referral gynecology practice. Institutional review board exemption was granted by Northside Hospital because of the retrospective nature of this study. Basing our definition of a parasitic myoma on the historical definition, we included only myomas that were completely separate from the uterus and obtained their main blood supply from another source.
Demographic data; surgery date; indications for surgery; number, dates, and types of prior surgeries; prior use of morcellation; locations of parasitic myomas; previous medical conditions; pathology; postoperative course; and follow-up were systematically retrieved from patient medical records. Intraoperative findings were correlated with pathologic findings. All specimens were evaluated by a staff pathologist and found to be leiomyomas.
Laparoscopic evaluation confirmed the presence of intraperitoneal and retroperitoneal myomas distinct from the uterus in 12 patients. The average age at diagnosis was 38.7 years (range 26–50 years), average parity was 0.25 (range 0–2), average number of prior surgeries was 2 (range 0–3 surgeries), average time between prior abdominal surgery and surgery during which a parasitic myoma was diagnosed was 75 months (range 2–204 months) (Table 1).
Intraoperative findings were correlated with histopathology to confirm “leiomyoma” in 11 of the 12 patients. One patient was noted intraoperatively to have a parasitic myoma on the sigmoid colon, and due to the intraoperative sequence of events, morcellation took place after removal of all leiomyomas, thus the pathologic specimen of the parasitic myoma was sent with other uterine myomas. In this case, pathology confirmed “leiomyoma” for the entire specimen.
Eighty-three percent (10 of 12) of patients had prior abdominal surgery. Sixty-seven percent (8 of 12) had a prior myomectomy—six performed laparoscopically, two performed by laparotomy. The six patients who underwent laparoscopic myomectomy involved morcellation. Two patients had undergone hysterectomy before diagnosis of the parasitic myomas. Interestingly, one patient had no evidence of uterine myomas despite confirmation of an isolated parasitic leiomyoma on the rectovaginal septum. Three patients were found to have multiple parasitic myomas, thus in our series, 15 myomas were found among 12 patients—each of the patients with multiple parasitic myomas had a prior laparoscopic myomectomy with morcellation. The majority (93%, 14 of 15) of myomas were found in the pelvis, including two retroperitoneal myomas, one of which was embedded in the bladder. Six of 15 myomas were found along the gastrointestinal tract, and 1 of 15 was found in the upper abdomen.
Since Kelly and Cullen wrote of parasitic fibroids in 1909,3 two theories for their pathogenesis have arisen. The first suggests that parasitic myomas are a rare variant of pedunculated subserosal myomas that have outgrown their uterine blood supply and become separated from the uterus, receiving blood supply from another source.3,4 More recently, a second theory has evolved which suggests “iatrogenic” parasitic myomas may be caused by the seeding of portions of fibroids during morcellation at the time of myomectomy or hysterectomy.6–8 The thought is that morcellation increases the possibility of leaving behind small fragments of myoma that go on to implant onto normal tissue anywhere in the peritoneal cavity. The incidence of iatrogenic parasitic myomas in the literature has increased since the introduction of laparoscopic techniques, and as noted in our case series, prior laparoscopic surgery seems to be a significant risk factor for the development of parasitic myomas.6–11
This case series reveals several interesting trends, suggesting possible risk factors and causes for parasitic myomas. The greatest risk factor for the development of parasitic myomas is the presence of uterine leiomyoma. However, it is notable that in fact one patient did not have any evidence of uterine fibroids. Patient 10 presented with a chief complaint of pelvic pain and was subsequently found to have a parasitic myoma on her rectovaginal septum, in close proximity to the lower uterine segment, but distinctly separate. The patient’s history was significant for one prior surgery for laparoscopic treatment of endometriosis, with no evidence on ultrasonography, hysteroscopy, or laparoscopy of uterine myomas. Such a finding begs the question of the myoma’s pathogenesis, and if in fact a third theory is possible for the cause of these rare myomas. Although this myoma could have once been a pedunculated myoma that lost its uterine blood supply, it is relevant here to consider the heterogeneous theories for leiomyoma and other smooth muscle neoplasm formation, including vascular spread as theorized in cases of intravascular leiomyomatosis and benign metastasizing leiomyomatosis and de novo formation from smooth muscle metaplasia of pluripotential cells as theorized in cases of leiomyomatosis peritonealis disseminata.12,13
The next most frequent risk factor is a history of prior morcellation of the uterus or myomas. In our series, 50% (6 of 12) of patients had a previous laparoscopic surgery involving morcellation. As previously described by various authors, this is not a novel association.6–10 However, given the high rate of association, and the biologic plausibility of this relationship, it is important that gynecologic surgeons consider the increased risk of parasitic myoma formation associated with morcellation of myomas at the time of myomectomy and similarly with morcellation of the uterus during hysterectomy. Notably, two patients in our series went on to develop parasitic myomas after abdominal myomectomy. With both laparoscopy and open procedures, attention to meticulous technique with complete removal of even small fragments of myoma is urged.
As suggested by case reports in the literature, our series reveals that the most likely locations of parasitic myomas are in areas “local” to a myomatous uterus. For example, Patient 1, who had no prior history of abdominal surgery, went on to have a large anterior abdominal wall myoma, weighing 791 g, which penetrated her rectus abdominus. This patient had preoperative magnetic resonance imaging of the abdomen and pelvis, which demonstrated a broad-based attachment of a subserosal fibroid (Fig. 1). Before surgery, she was found to have a 22-week-sized uterus and was treated with leuprolide (Lupron, Tap Pharmaceuticals, Deerfield, IL). By the time her abdominal cavity was assessed intraoperatively, this 13-cm leiomyoma had lost its attachment to the uterus and parasitized to her anterior abdominal wall (Fig. 2). The imaging, clinical presentation, and intraoperative findings support Brody’s hypothesis for the natural history of parasitic myoma development.4 That is, either spontaneously or through an agent that restricts blood supply to the myoma (eg, GnRH agonists, uterine artery embolization), a subserosal or pedunculated myoma may lose its uterine blood supply and “parasitize” to an adjacent organ.
The most common indication for surgery was pain, followed by uterine bleeding—nonspecific symptoms which were attributed to concomitant uterine myomas. Because these symptoms are more commonly associated with uterine myomas, the diagnosis of parasitic myomas was almost always incidental at the time of laparoscopy for management of what were perceived to be symptoms of uterine myomas. This again highlights the importance of systematic and thorough visual examination of the entire peritoneal cavity. The upper abdomen and retroperitoneal spaces (Fig. 3) are often obscured by other organs, and can be difficult to access; an exploration of these areas may be limited at the time of laparotomy, especially if performed through a minilaparotomy or Pfannenstiel incision. It is possible that these parasitic myomas, which could be overlooked, may be the cause of subtle symptoms, depending on location. Given the retrospective nature of this study, chart review suggests that the finding of a parasitic myoma could account for secondary complaints, such as constipation and dyschezia in the patient with sigmoid myomas, urinary frequency in the case of the patient with a posterior bladder myoma, and right lower quadrant pain in the patient with an appendiceal myoma (Fig. 4 and 5).
Review of our experience suggests that what had once been considered a benign, inevitable entity may be, at least in part, iatrogenically created and additionally, cause symptomatology. Preoperative planning remains an essential tool in the gynecologist’s arsenal; symptoms gathered during a thorough medical history that are not consistent with the patient’s physical examination findings should be investigated further. The use of ultrasonography and even magnetic resonance imaging or computed tomography scans may be beneficial in these cases in identifying an unanticipated mass. Given the association between morcellation and parasitic myomas, these observations hold especially true for patients who have had a prior uterine surgery, namely myomectomy or even hysterectomy.
Perhaps most importantly, this case series reiterates the fact that complete and thorough inspection of the abdominal cavity remains an important aspect of pelvic surgery. It has been our practice to thoroughly irrigate the entire abdominal cavity with approximately 3 L of lactated Ringer’s solution while alternating from Trendelenburg to reverse Trendelenburg positioning after all our procedures, thereby floating and dislodging any remnant tissue. Whether access is by laparotomy or by laparoscopy, meticulous attention should be paid to basic surgical principles, including attention to complete removal of small fragments of fibroid that may be buried under bowel or bladder or stuck in cannulas and wedged in the abdominal wall.
Although minimally invasive approaches have provided multiple benefits to patients and surgeons, we must continue to be vigilant about the potential complications and side effects of this approach, and we must be certain that we are not creating future problems while dealing with those at present.
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