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Amenorrhoea Secondary to Endometrial Ablation and Asherman's Syndrome Following Uterine Artery Embolization
CASE REPORT
6 Togashi M, Takizawa S, Okada S, Hoshiai H, Moriyama Y. Case of subserosal myoma of the uterus suspected as Meigs' syndrome. Naika-Int Med 1967;20:785±789. 7 Frank N, Frank MJ. Uterine tumor mimicking Meigs' syndrome. J Med Soc N J 1973;70:17±18. 8 Solomon S, Farber J, Caruso LJ. Fibromyomata of the uterus with hemotorax: Meigs' syndrome?. Arch Intern Med 1971;127:307±309.
317
9 Handler CE, Fray RE, Snashall PD. Atypical Meigs' syndrome and pseudo Meigs' syndrome. Thorax 1982;37:396±397. 10 Rush BM. Leiomyoma of the uterus, ascites and hydrothorax ( pseudo-Meigs' syndrome). J Louisiana State Med Soc 1976;128: 7±8. 11 Kim JC, Nam SL, Suh KS. Leiomyoma of the ovary mimicking mucinous cystoadenoma. J Clin Imaging 2000;24:34±37.
doi:10.1053/crad.2001.0846, available online at http://www.idealibrary.com on
Amenorrhoea Secondary to Endometrial Ablation and Asherman's Syndrome Following Uterine Artery Embolization C . D AV I E S*, M . G I B S O N *, E . M . H O LT {, E . P. H . TO R R IE * Departments of *Radiology, Royal Berkshire Hospital, Reading, U.K. and {Obstetrics and Gynaecology, Royal Berkshire Hospital, Reading, U.K.
Uterine artery embolization (UAE) is now a well-recognized treatment for uterine ®broids. We present a case complicated by endometrial ablation and Asherman's syndrome which has not previously been reported. CASE REPORT A 37-year-old Afro-Caribbean woman presented with a 3-year history of painful menorrhagia and primary infertility. Her menstrual cycle was regular. Four years previously she had undergone dilatation and curettage and a hysterosalpingogram which was normal. Clinical examination revealed a 12 to 14-week sized uterus. Biochemical investigations ( follicle-stimulating hormone) (FSH), luteinizing hormone (LH), oestradiol, testosterone, prolactin and thyroid function tests) were normal. Magnetic resonance imaging (MRI) showed a moderately enlarged uterus (298 ml) containing a number of submucosal and subserosal ®broids (dominant ®broid 37 ml) (Fig. 7). No ovarian abnormality was identi®ed. As the MRI demonstrated multiple ®broids it was felt that myomectomy would be technically dicult. The patient was counselled on the treatment options and elected to undergo UAE. Full informed consent was obtained. The risk of ovarian failure and the fact that fertility could not be guaranteed was explained. She underwent uneventful bilateral UAE. The uterine arteries were embolized until stasis was achieved using polyvinyl alcohol ( particle size 300±500 microns). The post-embolization course was initially uneventful. At her 3-month review she reported amenorrhoea. An ultrasound at that time showed a bulky uterus secondary to several ®broids, the largest measuring 3.5 cm. FSH and oestradiol were in the normal range (FSH 2.5, oestradiol 664). She was unsuccessfully treated with a course of medroxyprogesterone in an attempt to induce a withdrawal bleed. MRI showed a moderate reduction in uterine volume (254 ml) with multiple small ®broids and a 2.5 cm ®broid protruding into the upper part of the uterine cavity (22 ml) (Fig. 2). The patient was admitted for hysteroscopy which showed yellow necrotic endometrium. A ®broid was seen to bulge into the cavity from the left upper anterolateral wall obscuring the left tubal ostium. This was excised completely and several endometrial biopsies were taken. Histology showed infarcted endometrium bordered with hyalinized Author for correspondence and guarantor of study: Dr E. P. H. Torrie, Department of Radiology, Royal Berkshire Hospital, London Road, Reading RG1 5AN, U.K.
®brous tissue containing a scattering of chronic in¯ammatory cells. The ®broid consisted of infarcted material. No embolic material was identi®ed within the vessels in the ®broid or in the endometrium. MRI at 6 months showed no change in the size of the dominant ®broid but a reduction in the intensity of the endometrial signal compared to the previous MR image. She was given a course of oestrogen to attempt to stimulate endometrial regrowth. MRI showed a reduction in both uterine volume (155 ml) and the size of the dominant ®broid (19 ml) and a few areas of higher signal of the endometrium (Fig. 3). A hysteroscopy at 15 months revealed Asherman's syndrome: intrauterine adhesions with most of the cavity lined with scar tissue. Some normal endometrium was visible around the tubal ostia. Amenorrhoea persisted with normal hormone levels (FSH 6.7, oestradiol 222).
Fig. 1 ± Sagittal T2 weighted MR images pre-embolization. Multiple ®broids are demonstrated in the myometrium (short arrows). Normal high signal is seen in the endometrium/endometrial cavity (long arrow).
318
CLINICAL RADIOLOGY
Fig. 2 ± Sagittal T2 weighted MR images 3 months post-embolization. Low signal within the ®broids consistent with embolization (arrows). No high signal is demonstrated in the endometrium/endometrial cavity.
DISCUSSION
This patient was referred with menorrhagia, dysmenorrhoea and primary infertility. As she was felt to be unsuitable for myomectomy but desired uterus sparing treatment she underwent UAE [1±3]. Several known complications of UAE exist [4]. They can be divided into early and late. The early complications are those related to any angiographic procedure, for example haematoma, thrombosis and femoral artery damage. The later complications include the post-embolization syndrome characterized by malaise and borderline pyrexia. Other late complications include infection and amenorrhoea (sometimes due to ovarian failure) [5]. However, in this patient endometrial necrosis followed by Asherman's syndrome was diagnosed post-procedure. Asherman described the presence of single or multiple intrauterine adhesions often associated with amenorrhoea, particularly occurring after repeated curettage. The obliteration may be partial or complete and the location of the adhesions is variable. Several theories of the pathophysiology exist. Asherman believed that sustained myometrial contractions caused narrowing of the isthmus, resulting in adhesions between opposing endometrial surfaces [6,7]. Various ®lling defects are seen on hysterography. Venous extravasation and cornual blockage are commonly associated. Women undergoing UAE must be made aware that fertility cannot be guaranteed. They must be informed of the risks of ovarian damage due to ischaemia and Fallopian tube damage secondary to infection which may impact on fertility [8,9].
Fig. 3 ± Sagittal T2 weighted MR images 10 months post-embolization. Normal high signal is now seen in the endometrium/endometrial cavity around the tubal ostia corresponding to the later hysteroscopic ®ndings (long arrow).
Uterine artery embolization is not recommended as a treatment for infertility secondary to ®broids [8]. In our case embolization seems to have caused endometrial ablation and therefore exacerbated/compounded the clinical problem of infertility. To our knowledge endometrial ablation and Asherman's syndrome has not previously been reported. This has implications for the patient's future fertility. REFERENCES 1 Goodwin SC, McLucas B, Lee M, et al. Uterine artery embolisation for the treatment of uterine leiomyomata: mid-term results. JVIR 1999;10:1159±1165. 2 Bradley EA, Reidy JF, Foreman RG, et al. Transcatheter uterine artery embolisation to treat large uterine ®broids. Br J Obstet Gynaecol 1998;105:235±240. 3 Sisken GP, Stainken BF, Dowling K, Meo P, Ahn J, Dolen EG. Outpatient uterine embolisation for symptomatic uterine ®broids: experience in 49 patients. JVIR 2000;11:305±311. 4 Vashisht A, Studd JWW, Carey AH, et al. Fibroid embolisation: a technique not without signi®cant complications. Br J Obstet Gynaecol 2000;107:1166±1170. 5 Amato P, Roberts AC. Transient ovarian failure: a complication of uterine artery embolisation. Fertil Steril 2001;75:438±439. 6 Klein SM, Garcia CR. Asherman's syndrome: a critique and current review. Fertil Steril 1973;24:722±735. 7 Chapman K, Chapman R. Asherman's syndrome: a review of all the literature, and a husband and wife's 20-year world-wide experience. J R Soc Med 1990;83:576±580. 8 Clinical Recommendations on the Use of Uterine Artery Embolisation in the Management of Fibroids. London, U.K.: RCR and RCOG, 2000. 9 In: Templeton A, Cooke I, O'Brien PMS, eds. Evidence-based Fertility Treatment. London, U.K.: RCOG, 1998.
6 Togashi M, Takizawa S, Okada S, Hoshiai H, Moriyama Y. Case of subserosal myoma of the uterus suspected as Meigs' syndrome. Naika-Int Med 1967;20:785±789. 7 Frank N, Frank MJ. Uterine tumor mimicking Meigs' syndrome. J Med Soc N J 1973;70:17±18. 8 Solomon S, Farber J, Caruso LJ. Fibromyomata of the uterus with hemotorax: Meigs' syndrome?. Arch Intern Med 1971;127:307±309.
317
9 Handler CE, Fray RE, Snashall PD. Atypical Meigs' syndrome and pseudo Meigs' syndrome. Thorax 1982;37:396±397. 10 Rush BM. Leiomyoma of the uterus, ascites and hydrothorax ( pseudo-Meigs' syndrome). J Louisiana State Med Soc 1976;128: 7±8. 11 Kim JC, Nam SL, Suh KS. Leiomyoma of the ovary mimicking mucinous cystoadenoma. J Clin Imaging 2000;24:34±37.
doi:10.1053/crad.2001.0846, available online at http://www.idealibrary.com on
Amenorrhoea Secondary to Endometrial Ablation and Asherman's Syndrome Following Uterine Artery Embolization C . D AV I E S*, M . G I B S O N *, E . M . H O LT {, E . P. H . TO R R IE * Departments of *Radiology, Royal Berkshire Hospital, Reading, U.K. and {Obstetrics and Gynaecology, Royal Berkshire Hospital, Reading, U.K.
Uterine artery embolization (UAE) is now a well-recognized treatment for uterine ®broids. We present a case complicated by endometrial ablation and Asherman's syndrome which has not previously been reported. CASE REPORT A 37-year-old Afro-Caribbean woman presented with a 3-year history of painful menorrhagia and primary infertility. Her menstrual cycle was regular. Four years previously she had undergone dilatation and curettage and a hysterosalpingogram which was normal. Clinical examination revealed a 12 to 14-week sized uterus. Biochemical investigations ( follicle-stimulating hormone) (FSH), luteinizing hormone (LH), oestradiol, testosterone, prolactin and thyroid function tests) were normal. Magnetic resonance imaging (MRI) showed a moderately enlarged uterus (298 ml) containing a number of submucosal and subserosal ®broids (dominant ®broid 37 ml) (Fig. 7). No ovarian abnormality was identi®ed. As the MRI demonstrated multiple ®broids it was felt that myomectomy would be technically dicult. The patient was counselled on the treatment options and elected to undergo UAE. Full informed consent was obtained. The risk of ovarian failure and the fact that fertility could not be guaranteed was explained. She underwent uneventful bilateral UAE. The uterine arteries were embolized until stasis was achieved using polyvinyl alcohol ( particle size 300±500 microns). The post-embolization course was initially uneventful. At her 3-month review she reported amenorrhoea. An ultrasound at that time showed a bulky uterus secondary to several ®broids, the largest measuring 3.5 cm. FSH and oestradiol were in the normal range (FSH 2.5, oestradiol 664). She was unsuccessfully treated with a course of medroxyprogesterone in an attempt to induce a withdrawal bleed. MRI showed a moderate reduction in uterine volume (254 ml) with multiple small ®broids and a 2.5 cm ®broid protruding into the upper part of the uterine cavity (22 ml) (Fig. 2). The patient was admitted for hysteroscopy which showed yellow necrotic endometrium. A ®broid was seen to bulge into the cavity from the left upper anterolateral wall obscuring the left tubal ostium. This was excised completely and several endometrial biopsies were taken. Histology showed infarcted endometrium bordered with hyalinized Author for correspondence and guarantor of study: Dr E. P. H. Torrie, Department of Radiology, Royal Berkshire Hospital, London Road, Reading RG1 5AN, U.K.
®brous tissue containing a scattering of chronic in¯ammatory cells. The ®broid consisted of infarcted material. No embolic material was identi®ed within the vessels in the ®broid or in the endometrium. MRI at 6 months showed no change in the size of the dominant ®broid but a reduction in the intensity of the endometrial signal compared to the previous MR image. She was given a course of oestrogen to attempt to stimulate endometrial regrowth. MRI showed a reduction in both uterine volume (155 ml) and the size of the dominant ®broid (19 ml) and a few areas of higher signal of the endometrium (Fig. 3). A hysteroscopy at 15 months revealed Asherman's syndrome: intrauterine adhesions with most of the cavity lined with scar tissue. Some normal endometrium was visible around the tubal ostia. Amenorrhoea persisted with normal hormone levels (FSH 6.7, oestradiol 222).
Fig. 1 ± Sagittal T2 weighted MR images pre-embolization. Multiple ®broids are demonstrated in the myometrium (short arrows). Normal high signal is seen in the endometrium/endometrial cavity (long arrow).
318
CLINICAL RADIOLOGY
Fig. 2 ± Sagittal T2 weighted MR images 3 months post-embolization. Low signal within the ®broids consistent with embolization (arrows). No high signal is demonstrated in the endometrium/endometrial cavity.
DISCUSSION
This patient was referred with menorrhagia, dysmenorrhoea and primary infertility. As she was felt to be unsuitable for myomectomy but desired uterus sparing treatment she underwent UAE [1±3]. Several known complications of UAE exist [4]. They can be divided into early and late. The early complications are those related to any angiographic procedure, for example haematoma, thrombosis and femoral artery damage. The later complications include the post-embolization syndrome characterized by malaise and borderline pyrexia. Other late complications include infection and amenorrhoea (sometimes due to ovarian failure) [5]. However, in this patient endometrial necrosis followed by Asherman's syndrome was diagnosed post-procedure. Asherman described the presence of single or multiple intrauterine adhesions often associated with amenorrhoea, particularly occurring after repeated curettage. The obliteration may be partial or complete and the location of the adhesions is variable. Several theories of the pathophysiology exist. Asherman believed that sustained myometrial contractions caused narrowing of the isthmus, resulting in adhesions between opposing endometrial surfaces [6,7]. Various ®lling defects are seen on hysterography. Venous extravasation and cornual blockage are commonly associated. Women undergoing UAE must be made aware that fertility cannot be guaranteed. They must be informed of the risks of ovarian damage due to ischaemia and Fallopian tube damage secondary to infection which may impact on fertility [8,9].
Fig. 3 ± Sagittal T2 weighted MR images 10 months post-embolization. Normal high signal is now seen in the endometrium/endometrial cavity around the tubal ostia corresponding to the later hysteroscopic ®ndings (long arrow).
Uterine artery embolization is not recommended as a treatment for infertility secondary to ®broids [8]. In our case embolization seems to have caused endometrial ablation and therefore exacerbated/compounded the clinical problem of infertility. To our knowledge endometrial ablation and Asherman's syndrome has not previously been reported. This has implications for the patient's future fertility. REFERENCES 1 Goodwin SC, McLucas B, Lee M, et al. Uterine artery embolisation for the treatment of uterine leiomyomata: mid-term results. JVIR 1999;10:1159±1165. 2 Bradley EA, Reidy JF, Foreman RG, et al. Transcatheter uterine artery embolisation to treat large uterine ®broids. Br J Obstet Gynaecol 1998;105:235±240. 3 Sisken GP, Stainken BF, Dowling K, Meo P, Ahn J, Dolen EG. Outpatient uterine embolisation for symptomatic uterine ®broids: experience in 49 patients. JVIR 2000;11:305±311. 4 Vashisht A, Studd JWW, Carey AH, et al. Fibroid embolisation: a technique not without signi®cant complications. Br J Obstet Gynaecol 2000;107:1166±1170. 5 Amato P, Roberts AC. Transient ovarian failure: a complication of uterine artery embolisation. Fertil Steril 2001;75:438±439. 6 Klein SM, Garcia CR. Asherman's syndrome: a critique and current review. Fertil Steril 1973;24:722±735. 7 Chapman K, Chapman R. Asherman's syndrome: a review of all the literature, and a husband and wife's 20-year world-wide experience. J R Soc Med 1990;83:576±580. 8 Clinical Recommendations on the Use of Uterine Artery Embolisation in the Management of Fibroids. London, U.K.: RCR and RCOG, 2000. 9 In: Templeton A, Cooke I, O'Brien PMS, eds. Evidence-based Fertility Treatment. London, U.K.: RCOG, 1998.