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Original Report |
1 Department of Radiology, Section of Vascular and Interventional Radiology,
Northwestern University Medical School, Northwestern Memorial Hospital,
Feinberg Pavilion, 251 E. Huron St., Chicago, IL 60611.
2 Present address: Department of Radiology, Decatur Memorial Hospital, 2300 N.
Edward St., Decatur, IL 62526.
Received November 4, 2002;
accepted after revision January 14, 2003.
Address correspondence to R. K. Ryu
(rkryu{at}hotmail.com).
Abstract
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CONCLUSION. Although persistent loss of detectable arterial perfusion after uterine artery embolization occurs in some women, most patients reestablish arterial perfusion and do not develop symptoms of ovarian failure.
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Although uterine artery embolization successfully treats menorrhagia and bulk-related symptoms, this procedure may also have untoward effects on ovarian perfusion and function. Compared with large series [2, 3], recent studies have shown a higher than anticipated incidence of ovarian failure [4] and elevated levels of follicle-stimulating hormone after uterine artery embolization [5]. The cause of premature ovarian failure after uterine artery embolization remains unknown.
The objective of this study was to assess immediate and delayed vascular effects of uterine artery embolization on ovarian function and arterial perfusion. We hypothesize that loss of ovarian perfusion may be a transient phenomenon.
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All six women underwent pulsed-wave and color Doppler transvaginal sonography immediately before and after uterine artery embolization as part of a separate study to assess ovarian arterial perfusion. These six women had complete loss of ovarian arterial perfusion after uterine artery embolization. The details and results of this separate periprocedural sonographic study are described elsewhere in detail [6]. The patients subsequently underwent an identical sonographic study several months later. Both prospective studies were approved by the institutional review board, and informed consent was obtained from all patients.
Imaging
The delayed sonographic studies were performed in an identical fashion to
the periprocedural studies, using the same sonographic equipment with
identical gain settings (Sequoia, Acuson, Mountain View, CA) by the same
senior technologist. A 5-MHz transvaginal probe was used in all patients.
Intraparenchymal ovarian arterial perfusion was assessed with pulsed-wave and
color Doppler sonography. Resistive and pulsatility indexes were calculated
and compared with periprocedual values
(Table 1). The same ovary that
had shown loss of perfusion immediately after embolization (three patients
with right ovarian artery, three with left ovarian artery) was identified on
the delayed sonographic studies.
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Questionnaires
At the time of follow-up, we evaluated each patient's ovarian function
after the uterine artery embolization using a standard set of questions.
Specifically, we asked patients whether they had experienced amenorrhea or
onset of new menopausal symptoms including night sweats, hot flashes,
emotional lability, or vaginal dryness after embolization.
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Questionnaires revealed that only one (17%) of the six patients experienced onset of new menopausal symptoms. She developed persistent amenorrhea, night sweats, and hot flashes immediately after embolization. This patient was one of two women who showed continued loss of ovarian arterial perfusion on delayed sonography. She was also the only woman more than 45 years old. She was one (33%) of three patients embolized with 350- to 500-µm polyvinyl alcohol particles. The other patient who had complete loss of ovarian arterial circulation resumed normal menses after the procedure and did not experience any menopausal symptoms at the time of follow-up. The four women with reestablished perfusion did not report amenorrhea or any other perimenopausal symptoms.
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Because resistive and pulsatility indexes reflect vascular impedance, reduced values indicate decreased resistance to ovarian arterial perfusion, as compared with preprocedural values. The cause of decreased impedance in these women is unclear. Nikolic et al. [7] described a technically successful uterine artery embolization that was a clinical failure because of perfusion of fundal leiomyomas by enlarged ovarian arteries. These researchers speculate that the ovarian arteries enlarged after embolization to compensate for uterine ischemia. This vascular alteration could also account for the decreased resistive and pulsatility index values seen in all four patients with reestablished ovarian arterial perfusion on delayed sonography.
One woman in our study remained amenorrheic, with the onset of menopausal symptoms immediately after embolization. This patient was the only subject in our study who was more than 45 years old. Other reported cases have suggested an age-related correlation to embolization-induced ovarian failure, with none of the patients less than 45 years old [4, 8]. A previous study reported ovarian failure in nine (43%) of 21 women more than 45 years old and in none of the women less than 45 years old who underwent uterine artery embolization [4]. Similarly, Spies et al. [5] studied follicle-stimulating hormone levels in 63 women before uterine artery embolization and at 3 and 6 months later. Although no significant change in basal hormonal levels occurred for the group as a whole, an increase in hormonal level exceeding 2 SDs from the basal level was seen at 6 months in seven patients, all of whom were more than 45 years old. The researchers concluded that in patients 45 years old or older, there was approximately a 15% chance of an increase in the basal hormonal level into the perimenopausal range 6 months after embolization. These findings support an age-related susceptibility to early menopause in women undergoing uterine artery embolization.
One patient in our study showed persistent absence of ovarian arterial perfusion on delayed sonography but continued to have regular menses and was free of menopausal symptoms. The most likely explanation is that because only one ovary could be identified, the other nonvisualized ovary had normal, undisturbed arterial perfusion. There is also the possibility that adequate arterial perfusion may be maintained but is beyond the resolution of current Doppler sonography technology to accurately reveal.
The anatomy of the uterine and ovarian arteries suggests that nontargeted embolization of the ovarian arteries is a possible mechanism for postprocedural ovarian failure. At the junction of the uterus and the fallopian tubes, the uterine artery turns laterally toward the ovary and terminates by anastomosing with the ovarian arterial system. These uterine–ovarian arterial anastomoses are seen in only 11% of patients [9]. Unilateral uterine arteriography can result in filling of the ipsilateral ovarian artery as well as the contralateral ovarian and uterine arteries, again pointing to the rich network of collaterals between the uterus and the ovaries [10]. The formation of collaterals in the female pelvis after embolization may indirectly contribute to subsequent ovarian failure. One potential explanation is the resultant creation of a vascular steal phenomenon with loss of autoregulatory mechanisms, in which blood is shunted preferentially toward the newly ischemic uterus, resulting in an ischemic and ultimately dysfunctional ovary.
Premature ovarian failure is not specific to uterine artery embolization. A rate of hysterectomy-induced ovarian failure similar to that of uterine artery embolization has been shown [11], suggesting local postsurgical hormonal derangement as a contributing factor. In another study, comparison was made between ovarian failure and the ages of 90 women who had undergone hysterectomy with bilateral ovarian conservation and 226 women who had undergone spontaneous menopause. The mean age (± SD) of women with ovarian failure in the hysterectomy group was 45.4 ± 4.0 years, which was significantly lower than the mean age of 49.5 ± 4.04 years in the nonhysterectomy control group [12]. This study suggests that the disruption of the hormonal milieu can be subtle in terms of overall impact on ovarian function: ovarian dysfunction may be subtotal. The exact cause of ovarian failure is unknown, regardless of procedure. Despite our findings, ischemia may play only a small or contributory role.
There were several important limitations to this study. First, the original sample size was small. To confirm our preliminary results, we need to perform studies with larger numbers of patients—patients who are younger than 45 years old and those who are 45 years or older. A multiinstitutional study would more rapidly accumulate enough patients with postprocedural ovarian failure to draw statistical conclusions. Second, our study does not have hormonal levels to correlate with sonographic findings. We do not routinely draw follicle-stimulating hormone levels prospectively because we do not believe hormone levels substantially affect fibroid management decisions. Therefore, we did not draw them during the time of the delayed study either. Third, sonography may not be the best imaging method with which to assess ovarian perfusion. Arteriography is a more direct imaging modality but subjects women to the risks of an invasive procedure. MR imaging is noninvasive, and its multiplanar imaging capability and soft-tissue contrast may more accurately reveal changes in ovarian circulation than can sonography. Finally, our study did not have a hysterectomy control group. It would be helpful to compare the incidence of ovarian failure in an age-controlled embolization group and in women who have undergone hysterectomies to determine whether uterine artery embolization increases susceptibility for premature ovarian failure.
In conclusion, although nontargeted embolization of the ovaries occurs during uterine artery embolization, most patients in our small sample reestablished ovarian arterial perfusion and continue to menstruate normally without appreciable menopausal symptoms. Women more than 45 years old seem to be predisposed to postembolization ovarian failure. The exact cause of postembolization ovarian failure remains unknown but is most likely multifactorial. An age-controlled comparative study of the incidence of postembolization and posthysterectomy ovarian failure is needed to better understand this phenomenon.
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This article has been cited by other articles:
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  J. M.P. Jaraquemada Possibility of hidden damages with temporary uterine artery occlusion device Hum. Reprod., October 1, 2006; 21(10): 2721 - 2721. [Full Text] [PDF]
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