Literature DB >> 28191151

Pregnancy after uterine arteriovenous malformation-case series and literature review.

Rebeka Eling1, Alison Kent2, Meiri Robertson3.   

Abstract

Purpose: To perform a retrospective audit of cases of uterine arteriovenous malformations (UAVM) at The Canberra Hospital and review of recent literature reporting pregnancies occurring after the diagnosis of UAVM aiming to devise a diagnostic and treatment protocol to optimise pregnancy post UAVM.
Methods: A retrospective audit of cases of UAVM at the Canberra Hospital from a prospectively managed patient database was performed. A search of the electronic database PubMed, for articles between 2000-2011 relating to pregnancy post UAVM. Individual case studies were analysed separately to case series.
Results: The study included 28 individual studies and five case series (61 women). Average age was 29.5 ± 6.7 (range 18-42). Most women (24, 85.7%, 100% in case series) presented with abnormal vaginal bleeding; 11 (41%) individuals presented post interruption of pregnancy. All women had had a previous pregnancy (mean gravidity 3.1 ± 3.1, range 1-15 for case studies) and only four women (14.2 %) had no history of uterine trauma. Only one woman (3.6 %) did not have any ultrasound and most women underwent colour Doppler ultrasonography (20, 71.4% in case studies; 61, 83.6% in case series). Of the women, 72 (53.6 % of case studies, 78.1 % of case series) were treated with uterine artery embolisation, seven (25%) were treated expectantly. A total of 63 pregnancies occurred post treatment, seven (13.9%) ending in miscarriage. Average time to conceive post diagnosis was 19 months ± 16.3 (range 2-72). A total of 54 healthy infants were born to mothers post AVM diagnosis.
Conclusion: UAVM are likely to exist on a continuum with other pregnancy related pathologies, such as sub involution of the placental bed, making a single best diagnostic and treatment plan difficult. However, this study shows that successful uncomplicated pregnancy is achievable for women after the diagnosis of UAVM.

Entities:  

Keywords:  pregnancy; ultrasound; uterine arteriovenous malformation

Year:  2015        PMID: 28191151      PMCID: PMC5025090          DOI: 10.1002/j.2205-0140.2012.tb00012.x

Source DB:  PubMed          Journal:  Australas J Ultrasound Med        ISSN: 1836-6864


Introduction

Uterine arteriovenous malformations (UAVM) are abnormal connections between uterine arteries and veins. UAVM can be congenital or acquired/traumatic. The clinical presentation of UAVM are variable–the classical clinical feature is intermittent, heavy vaginal bleeding, which can be life threatening. UAVM can also be fairly asymptomatic. The incorporation of necrotic villi in the venous sinuses of scar tissue is thought to cause acquired UAVM. An acquired UAVM almost always occurs after a uterine trauma, such as dilation and curettage or caesarean section but can also be associated with normal vaginal birth or malignancy. UAVM may also be congenital, occurring rarely in the uterus, and usually invading surrounding structures. Congenital lesions classically present with severe menorrhagia, unresponsive to conventional therapy. UAVM can be diagnosed with grey scale and colour Doppler ultrasonography, MRI and CT angiography; radiographic angiography remains the gold standard. There can be considerable overlap in the presentation and appearance of UAVM and other pathologies related to pregnancy and uterine trauma, such as sub involution of the placental bed (SPB), retained products of conception (RPOC) and gestational trophoblastic disease (GTD). UAVM can also occur concurrently with or post resolution of a spontaneous incomplete miscarriage as well as trophoblastic disease. Accurate diagnosis is critical, as the treatment for RPOC and GTD (generally dilation and curettage) is contraindicated in UAVM, as there is the risk of causing massive haemorrhage and death. UAVM are characterised by a negative beta human chorionic gonadotrophin (BHCG) value, which is usually weakly elevated in RPOC and grossly elevated with GTD. RPOC, GTD, UAVM and SPB can present with vaginal blood loss or haemorrhage, – with RPOC and SPB exclusively occurring post pregnancy. , GTD and UAVM can be discovered during or post pregnancy. , UAVM appear as multiple anechoic spaces in the myometrium (Figure 1), with a typical spectral Doppler appearance of turbulent flow (Figure 2), low resistance, high velocity. A colour mosaic pattern is seen with colour Doppler imaging. A key feature is that the colour Doppler images are vastly more informative than the grey scale imaging. SPB appear similar to UAVM. RPOC are seen on ultrasound as a focal echogenic mass in the endometrium with low resistance flow , while GTD has anechoic spaces and an absence of a fetus.
Figure 1

2D grey scale images of an UAVM–note the multiple anechoic spaces.

Figure 2

Colour Doppler image demonstrating turbulent flow creating a mosaic pattern.

2D grey scale images of an UAVM–note the multiple anechoic spaces. Colour Doppler image demonstrating turbulent flow creating a mosaic pattern. Standard of treatment for UAVM was previously hysterectomy, current fertility preserving techniques, mainly uterine artery embolisation (UAE), are becoming more widely accepted. The uterine artery is embolised with micro particles, coils, glue or alcohol, while collateral supply maintains uterine perfusion, thus preserving fertility. , There have been several case studies of pregnancy after embolisation for UAVM in the literature, but only a few reviews, and no classification scheme for best diagnostic methods and outcome incorporating clinical presentation and past medical history. This paper aims to review the literature and add a retrospective audit of a further case series to devise a diagnostic and treatment protocol for maximising fertility post UAVM.

Methods

Search strategy

The PubMed search engine was used, searching for English articles, between 1st January 2000 and 30th June 2011 with the search terms “uterine arteriovenous malformation”. A MeSH search was also performed, using terms “uterine”, “arteriovenous malformation” and “arteriovenous fistula”. Cases where a pregnancy occurred after diagnosis and/or treatment of an UAVM as well as cases where UAVM was diagnosed and treated during a pregnancy were included in the current study. Articles pertaining to congenital UAVM were excluded. Case studies and series were used, although only case series in which sufficient individual patient data could be extracted were used in pooled calculations. Case series where there were insufficient individual data were collated separately. Cases where UAVM were diagnosed or treated during a pregnancy were included for completeness, but were not used in the frequency calculations

Retrospective case series

Thirteen women were diagnosed with uterine UAVM in the Fetal Medicine Unit (FMU) at The Canberra Hospital (TCH), Canberra, between 2000–2011. Only those patients who conceived post diagnosis were included in the current study. Ethics approval for the study was obtained from the ACT Health Human Research Ethics Committee (ETHLR. 11.122).

Data

From both the literature and the cases seen at TCH, the following data was extracted (where it was supplied): author's names, date of publication, patients age, gravity and parity at time of diagnosis, brief summary of presenting complaint (menorrhagia, haemorrhage, abnormal vaginal bleeding), relevant past medical history (mainly obstetric history and uterine trauma), BHCG levels at time of treatment, diagnostic methods, size of AVM, length of time between AVM diagnosis and uterine trauma, treatment, number of UAE procedures, description of UAE procedures, embolic agent used, which uterine artery embolised (right, left or both), was the AVM diagnosed during a pregnancy, spontaneous pregnancy losses post treatment, how long was the time to conceive post treatment, at what gestation was the subsequent pregnancy delivered, what type of delivery (vaginal, forceps or caesarean), complications of pregnancy/delivery (including problems conceiving or “minor” labour complications such as perineal tears), infant weight, sex and Apgar score and relevant follow up. The data was tabulated, and averages, medians and ranges were calculated for relevant data. Percentages were also calculated using Microsoft Excel (Microsoft Co, Seattle WA, USA).

Suggested diagnostic and treatment mechanism

A flow chart was devised, based on the patients seen through the Fetal Medicine Unit at the Canberra Hospital.

Results

Initial PubMed search yielded 112 articles. Of these, there were 86 cases or case series regarding acquired AVMs, with 25 reporting cases that resulted in pregnancy. Of the articles reporting pregnancy, 17 were case studies and eight were case series. Of the case series, three had enough data on individual patients to include in individual analyses, resulting in 24 patients from the literature, two of which were pregnant at the time of treatment. Six patients were seen through the FMU, resulting in 28 individual patients included in calculations (Table 1).
Table 1

Summary of key patient data.

Reference Age Gravidity Parity Presentation PMH Time since trauma
Rebarber13A 34Multi gravidaVaginal Bleeding @ 20 wks.2 LUSCS and scar separation
Castro–Aragon24A 29G1P0Routine antenatal scanMyomectomy, fibroids
Kelly 25 27G3P0Routine antenatal scan (pregnancy ended in SA)GTD, MTX and suction curettage, D&C for SA2 m
Nasu 26 27G1P0Premature labour at 21 wksAsymptomatic Ix for ovarian dysfunction
Reyftmann 27 %28G1P1Secondary amenorrhea post deliveryNVD, 4 menses since4 m
Gopal 28 42G6P0Infertility investigationsInfertility, D&C 1 IP, 4 SANG
Delotte 29 33G2P0Metorrhagia, 6 monthsOvarian infertility, IP(medical), several BT18 m
Przybojewski 14 21G8P4PV bleeding 1 week and menorrhagia2 D–C for PV bleeding2 m
Tsai 30 305–6yr hx or irregular excessive bleeding3 SA, 1 MPNG
Nikolopoulos 31 39G1P0PV post SASA (evacuation), BT8 w
Chia 32 37G3P2Profuse PV post SASA, D&C, menometorrhagia rx with tranexamic acid, 2 LUSCS, BT3 m
Dar4* 26G1P1Profuse PVTraumatic cervical dilationNG
Garner 33 31G1P0Heavy PV after cessation of OCPD&C, GTD rx 6xMTX 1 year prior
Amagada 34 17G1P0PV bleeding post1 w
Goldberg 35 34G15P3PV post IP8 IP3 y
Nonaka 36 30G1P0PV post IPIP at 16 weeks1 m
Onoyama 37 22G2P0PV post IPIP4 w
McCormick 38 30G7P3PV post IPBT (2units)3 m
Kim 39 35G4P2PV post IP2 D&C, C/S4 m
Timmerman 3 27* G1P0PV post IPIV oxytocin and ergometrin, repeat D*C6 w
29G3 P1+2PV post IPLate IP for foetal deathNG
19G2P1+1Massive PV and painPlacenta accreta, PPH, rx ergometrin, BT (2 units)2 w
36G3P0+3PV post IPRPOC and fibroidsNG
NGG1P0+1PV post IPIP at 20 wks.6 w
FMU Pt 131G4P2PV post SA2 normal pregnancies, NVD, genital herpes, IP, D+C1 y
FMU Pt 234G3P0PV post IP2 × IP3 m
FMU Pt 335G2P1PV post IPLUSCS, D+C2 w
FMU Pt 429G4P0PV post SA3 SA, D+C
FMU Pt 518G1P1Heavy PV post LUSCSLUSCS (28 wks)3 w
FMU Pt 636G1P0Heavy PV post SAMenorrhagia, BT2 m
Degani, et al. 2009 12 pts, 6 preg24–34G1+Prolonged bleading, possible RPOC7 post TANG
Ghai, et al. 2003 15 pt, 5pret (4pts)23–43G1+Massive uterine bleeding10 pt D+C 4pt–uterine instrumentation1m–7yr
Lim, et al. 2002 14 pts, 4 preg18–43G1+Uterine haemorrhage14–GTD, BTNG
Maleux, et al. 2006 17pts, 6 preg25–38G1+Vaginal haemorrhage7–BT 13–D+C75d
Yang, et al. 2005 15 pts, 5 preg25–42G1+Massive vaginal bleeding15–>2 D+C or LUSCS 4–both3d–16m

Key: LUSCS–lower uterine segment caesarean section, PV–per vaginal bleed, CDUS–colour Doppler ultrasound, GSUS–grey scale ultrasound, TA–trans abdominal, TV–trans vaginal, MRI–magnetic resonance imaging, US–ultrasound, DUS–Doppler ultrasound, IP–interruption of pregnancy, GTD–gestational trophoblastic disease, RPOC–retained products of conception, MTX–methotrexate, MM–methylergonovine maleate, NVD–normal vaginal delivery, LFD,–lower forceps delivery,

Summary of key patient data. Key: LUSCS–lower uterine segment caesarean section, PV–per vaginal bleed, CDUS–colour Doppler ultrasound, GSUS–grey scale ultrasound, TA–trans abdominal, TV–trans vaginal, MRI–magnetic resonance imaging, US–ultrasound, DUS–Doppler ultrasound, IP–interruption of pregnancy, GTD–gestational trophoblastic disease, RPOC–retained products of conception, MTX–methotrexate, MM–methylergonovine maleate, NVD–normal vaginal delivery, LFD,–lower forceps delivery,

Patients

The mean age of women diagnosed with AVM was 29.5 +/−6.7 SD, range 18–42 years. The mean gravity was 3.1 ± 3.1 SD (range 1–15) and parity was 0.81 ± 1.2 SD (range 0–3). The most common presenting complaint was per vaginal bleeding (24/27–85.7%). Eleven women (39.3%) presented with vaginal bleeding post interruption of pregnancy and six women (21.4%) presented with bleeding post spontaneous miscarriage. Two women (7.1%) presented post‐delivery (one normal vaginal delivery and one caesarean section delivery). Three women (10.7%) presented with chronic menorrhagia or metorrhagia. UAVM were also diagnosed incidentally during infertility investigations or on a routine antenatal scan in two women (7.1%). Fourteen women (50%) had a past medical history including interruption of pregnancy; eight women (28.6%) had a dilation and curettage (D&C) procedure. Four women (14.3%) had one or more caesarean delivery and three (10.7%) had been treated for molar pregnancy ± gestational trophoblastic disease (GTD). The average time since uterine trauma was 144.9 days (range 7–1095, SD ± 258.9). BHCG levels at time of diagnosis were not reported for 16 women (57.1%), with nine women (32.1%) having a negative BHCG and three women (10.7%) reported as having a positive BHCG level (Table 2).
Table 2

Patient data, past medical history, diagnosis and treatment.

Parameter Median / Range or Number / Percentage
Patients–28
Age (years)30/18–42
Gravity32/1–15
Parity0/0–4
Presenting complaint
Per vaginal bleeding24/85.7%
Post TA11 / 39.3%
Post SA6/21.4%
Post delivery2/7.1%
Menorrhagia / metorrhagia3/10.7%
Other / unspecified2/7.1%
Infertility investigations / incidental2/7.1%
Secondary amenorrhea1/3.6%
Routine antenatal scan1/3.6%
Past medical history
TA14/50%
D&C8/28.6%
LUSCS4/14.3%
Infertility3/10.7%
GTD/MP3/10.7%
Other–CIN ii, fibroids4/14.3%
No uterine trauma4/14.3%
Time since uterine trauma (days)60/7–1095
BHCG
Not given16/57.1%
Negative9/32.1%
Diagnostic methods
Any type of ultrasound27/96.4%
Ultrasound (unspecified)4/14.3%
Transvaginal ultrasound9/32.1%
Transabdominal ultrasound7/25%
Grey scale ultrasound14/50%
Doppler ultrasound (unspecified)2/7.4%
Colour doppler ultrasound20/71.4%
Power doppler ultrasound1 / 3.6%
Mri / mr angiography7/25%
CT1 / 3.6%
Angiography17/60.7%
Other4/14.3%
Size of lesion–max width (mm)40/26–67.5
Treatment
UAE15/53.6%
Expectant / none7/25%
Medical5/17.9%
Surgery1 / 3.6%
Hysteroscopy1 / 3.6%
UAE procedures–15 pts, 18 procedures
Number of procedures per patient1/1–2
Embolic agent
Pva / particles7/48.9%
Glue /nbca2/11.1%
Coils / micro coils4/22.2%
Gelfoam / gelatine sponge4/22.2%
Histoacryl and I4/22.2%
Alcohol1 / 5.6%
Not given6/33.3%
Positive3/10.7%
Patient data, past medical history, diagnosis and treatment.

Diagnosis

The most commonly reported modality used in diagnosis was colour Doppler ultrasound (CDUS), with 20 women (71.4%), followed by grey scale ultrasound (GCUS) which was performed in 14 women (50%). Power Doppler was performed in one woman (3.6%), 17 women (60.7%) underwent angiography and seven (25%) were diagnosed with magnetic resonance imaging or angiography (MRI/MRA). Other diagnostic modalities include CT (one woman, 3.6%). Four women (14.3%) were diagnosed with other modalities (e.g. hysterosalpingogram or laparoscopy). The average maximal width of the lesion (when reported) was 41.1 mm ± 14.8 SD (range 26–67.5 mm) (Table 3).
Table 3

Pregnancy and Infants post UAVM diagnosis.

Pregnancies–36
Time to conceive post dx/rx (months)14/2–72
Delivery
Normal vaginal delivery10/257.8%
Lower forceps delivery2/5.6%
Caesarean section delivery9/25%
Complications miscarriage5/13.9%
Antenatal8/22.2%
Postnatal5/13.9%
None10/27.8%
Not given2/5.6%
Infants–32
Gestation39w / 28w2d–41w
Weight (g)3081 / 1140–4015
Sex
Male11 / 34.4%
Female11 / 34.4%
Not given9/28.1%
Apgar
1 minute8/2–9
5 Minute9/8–10
Pregnancy and Infants post UAVM diagnosis.

Treatment

Uterine artery embolisation (UAE) was performed in 15 women (53.6%). Seven women (25%) were managed expectantly, with no treatment. Five women (17.9%) were medically treated, most commonly with methylergonovine (three women, 10.7%). One woman (3.6%) had the lesion surgically excised and one woman (3.6%) had hysteroscopic removal of retained products of conception (RPOC) which also resolved her AVM. UAE–uterine artery embolisation, BT–blood transfusion, SA–spontaneous abortion (miscarriage), Ang–angiography, D&C –dilation and curettage, Ix–investigations, OCP–oral contraceptive pill, NG–not given, ^–diagnosis of UAVM during a pregnancy, data not included in calculations *–patients went on to have multiple pregnancies post diagnosis of UAVM $–Patient did not go on to have a successful pregnancy, but did conceive post UAVM diagnosis Of the women, 15 had a total of 18 UAE procedures, with the average number of procedures per patient being 1.2 ± 0.4 SD (range 1–2). The most commonly used embolic agent was PVA or other particles (seven procedures, 48.9%). Other embolic agents included: Glue/NBCA (two procedures, 11.1%), coils or micro coils (four procedures, 22.2%), gel foam or gelatines sponge (four procedures, 22.2%), histoacryl and lipiodol (four procedures, 22.2%) and alcohol (one procedure, 5.6%). Embolic material was not given for six (33.3%) of procedures (Table 3).

Pregnancies

The 28 patients included in the study had a total of 35 pregnancies. Five of these pregnancies (13.9%) ended in miscarriage after diagnosis and/or treatment of the UAVM. The average time to conceive post diagnosis/treatment was 19 months ± 16.3 SD (range 2–72 months). Nine (25%) pregnancies resulted in caesarean delivery, ten in normal vaginal delivery (27.7%) and two (5.6%) instrumental deliveries. Eight of the pregnancies (22.2%) had antenatal complications(including difficulties conceiving and premature labour) and five (13.9%) had postnatal (e.g. postpartum haemorrhage) complications. Ten pregnancies (27.8%) reported no complications either antenatally or postnatally. The average gestation for pregnancy post UAVM was 264.8 days (range 198–281, SD ± 23.4) (Table 4).
Table 4

Case series analysis parameters.

Median / Range or Number / Percentage
Studies
Number of patients (total = 73)15/12–17
Number of pregnancies (total = 28)6/4–6
Number of infants (total = 22)5/0–6
Age (median of average)31.4/18–43
Presenting complaint
Vaginal haemorrhage73/100%
Past medical history
Dilation and curettage35/47.9%
Therapeutic abortion8/11.0%
LUSCS6/8.2%
GTD22/30.1%
Other16/21.9%
BHCG
Not given/performed29/39.7%
Negative30/41.1%
Positive14/19.2%
Diagnosis
Ultrasound29/39.7%
GSUS15/20.5
CDUS61/83.6%
MRI6/8.2%
Angio45/61.6%
Other–hysteroscopy, histopathology, etc13/17.8%
Treatment
UAE57/78.1%
Hysterectomy4/5.4%
Not specified12/16.4
Embolisation 85 procedures in 61 patients
>1 procedure14/24.6%
Embolic agent
PVA30/35.3%
Particles7/8.2%
Glue12/14.1%
Coils8/9.4%
Gelfoam10/11.8%
Dura mata1/1.2%
Side
Not given16/18.8%
Left8/9.4%
Right1/1.2%
Pregnancies n = 28
Normal term delivery19/67.9
LUSCS1/3.6%
Termination4/14.3
Miscarriage2/7.1
Case series analysis parameters.

Infants

There were 32 live infants from the 36 pregnancies, with two women (5.6%) conceiving twins, one woman (2.8%) having two children post diagnosis and one woman (2.8%) having three children. The average birth weight was 2969 g (range 1140–4015, SD ± 1123.6). There were 11 males (34.4%) and 11 females (34.4%) born (nine studies (28.1%) did not report infant sex). Mean Apgar scores at one and five minutes were 6.6 and 9.0 respectively (see Table 4).

Case series

Five case series did not have enough data to individually analyse patients that became pregnant. These cases were grouped and analysed, resulting in 73 patients, 28 of which became pregnant, resulting in 22 infants. The patients ranged in age from 18–43, and all had a gravidity of at least one. The presenting complaint for all patients in the case series was vaginal haemorrhage. Thirty‐five patients (47.9%) had a history of D&C, 8 (11%) or therapeutic abortion and 6 (8.2%) of LUSCS. Twenty‐two patients (30%) had a history of GTD, a bias accounted for by one of the papers, which exclusively looked at patients with UAVM resulting from GTD. BHCG was not performed or given in 29 (39.7%) patients, and was negative in 30 (41.1%). BHCG was positive in 14 (19.2%) patients, again accounted for by the study focussing on GTD. Diagnosis was achieved by CDUS in 61 patients (83.6%) and by angiography in 45 patients (61.6%). Treatment was predominantly UAE (61 patients, 83.6%), with 14 patients (24.6%) requiring more than one embolisation procedure. The most common type of embolic material was PVA (30 patients, 35.3%), followed by glue (12 patients, 14.1%), gelfoam (10 patients, 11.8%) and coils (8 patients, 9.4%). Bilateral embolisation was done in 44 patients (51.8%) and the left uterine artery in 8 (9.4%) of patients. Most of the pregnancies (19, 67.9%), were ‘normal, term deliveries’, one (3.6%) was a LUSCS. Four patients (14.3%) had elective terminations of their pregnancies post embolisation, and two patients had miscarriages (7.1%). Suggested Diagnostic and Treatment Mechanism (Figure 3)
Figure 3

Spectral Doppler wave.

Spectral Doppler wave.

Discussion

Uterine arteriovenous malformations are a rare cause of abnormal vaginal bleeding, most commonly seen in women who have been pregnant and experienced some type of uterine trauma, such as D&C. UAVM can be difficult to diagnose, not only because they are rare, but because they may present similarly to, or in conjunction with, other pregnancy related pathologies, such as subinvolution of the placental bed, retained products of conception and gestational trophoblastic disease . It is important to make an accurate diagnosis of UAVM, as treatment for RPOC and GTD may include D&C, which is contraindicated in UAVM. Three women (10.7%) in the current study had a history of gestational trophoblastic disease, eight women (28.6%) had a history of at least one D&C and 14 women (50%) reported previous interruptions of pregnancy. Two women (7.1%) had a history of RPOC. None of the women in the current study were nulligravid and most women (24 / 85.7%) presented with per vaginal bleeding. The gold standard of diagnosis of UAVM is angiography, although colour Doppler ultrasound is now the most widely used first line of investigation. Angiography has the benefit of allowing treatment (in the form of embolisation) at the time of diagnosis. Sixteen women in the current study underwent angiography as a diagnostic modality, and all but one woman (27 / 96.4%) underwent some form of ultrasonography. It has been proposed by Timmerman, et al. that SPB and UAVM constitute a spectrum of disease rather than distinct pathologies. This could explain why some women are able to be treated medically, or why sometimes no treatment is needed, whilst in others, lifesaving embolisation of the uterine arteries is required. Timmerman suggests the term uterine vascular malformations for those diagnosed by ultrasound, with arteriovenous malformation describing only those lesions seen on angiography to have the appropriate characteristics (early venous filling). Aside from angiography, the clinical picture and ultrasonographic features of uterine vascular malformations are very similar: hyper vascular areas within the myometrium, showing turbulent, low resistance flow, often associated with varying degrees of vaginal bleeding. Therefore while arteriovenous malformations can be suspected with ultrasound, only angiography can differentiate true UAVM from potentially more benign vascular lesions. , Uterine artery embolisation has been used for many causes of vaginal bleeding, including UAVM, fibroids and postpartum haemorrhage. It is the preferred method because it has the potential to preserve fertility. In cases that require embolisation, there are a range of embolic materials which may be used. In this study, the most common embolic agent was particles (seven procedures, 48.9%). It does not appear that embolic agent choice has an impact on future fertility, as the 14 patients embolised in this study went on to have normal pregnancies, regardless of embolic material used. Although it is not possible to make conclusions from the current study, it seems likely that the clinical presentation and perhaps lesion size is more important than the embolic agent used for determining future fertility. This study is an important first step in looking at how to maximise fertility post diagnosis and treatment of UAVM. However, there are some weaknesses. First, it is hard to get all the details needed from the literature, as most cases are published as individual studies, each with a different focus (such as diagnostics or treatment), meaning other important details are omitted. Also, not all cases of UAVM will be documented in the literature, and only one database was searched in this study, which may possibly result in a publication bias. Second, this study is only looking at women who became pregnant post diagnosis and treatment; to make any definitive statements about diagnosis and treatment to maximise fertility, a comparison of these patients needs to be made with those who have had a diagnosis and treatment of UAVM and who have not become pregnant. This in itself would be difficult, as pregnancy is usually a conscious choice, not an invariable outcome. Other factors, such as patient age and other causes of infertility, will affect the rates of pregnancy post diagnosis and treatment of UAVM. Last, the diagnostic and treatment flowchart devised was based only on the six patients seen at the FMU, embolisation was required when the maximum diameter of the AVM was greater than 30 mm. Smaller lesion were either managed expectantly or supported with Tranexamic acid. It would not be appropriate to generalise this flowchart without further study. Suggested diagnostic and treatment flowchart based on patients seen at the Fetal Medicine Unit, The Canberra Hospital, Canberra.

Conclusion

In conclusion, UAVM are rare, potentially life threatening causes of vaginal bleeding that can be effectively treated with UAE, but some may also be safely managed conservatively. This study looked at 27 women, who became pregnant 34 times, giving birth to 31 infants post UAVM diagnosis. It is particularly reassuring that there were no catastrophic complications of pregnancy and labour post diagnosis, such as severe growth restriction or abnormal invasion of the placental bed (acereta) in this group of patients, and minor complications were limited. Ultrasound is a safe and reliable method for suggesting an UAVM, although angiography remains the gold standard for definitive diagnosis. UAVMs are likely to exist on a continuum with SPB, making it difficult to establish a single best diagnostic and treatment regime, although a possible mechanism has been suggested, based on the patients seen at this institution. Further studies to compare the women in the current study with those diagnosed with UAVM and who have not become pregnant, wider review of literature databases and perhaps collaboration between multiple centres would be useful in determining best course for diagnosis, treatment and fertility preservation in the setting of uterine UAVM.
Diagnosis Treatment TTC post Dx/Rx (m) SA post Rx Delivery Complications
TA/TV GSUS, CDUSUAENoLUSCSYes
GSUS, CDUSExpectantNoLUSCSNo
DUS, AngUAEYesLFDYes
US, MRI, MRA, Ang (postpartum)UAE24NoNVDYes
TA/TV GSUS Hysterosalpingogram CDUS, MRI, AngUAE14YesYes
Hysterosalpingogram, MRI/MRA, AngUAENoLUSCSYes
CDUS, AngUAE12NoNVDYes
GSUS, Ang, MRIUAE48Yes (8wks)NGYes
CDUS, AngUAE24NoNVDNo
DUS, Laparoscopy, hysteroscopy, AngSurgical removal of UAVM14NoLUSCSYes
US, PDUS, CT, AngUAE9NoLUSCSNo
GSUS, CDUS, AngUAE72NoNGNG
US, MRA, AngD&C, UAE15Yes (2)LFDYes
CDUS, AngTranexamic acid and Iron, UAE24NoNVDNo
CDUSMM36NoNVDYes
CDUS, MRIMM &leuroprelin5NoNVDNo
TV GSUS, CDUS, AngMM7NoLUSCSNo
US, MRI, AngUAE4NoNVDNo
CDUS, AngUAE36NoLUSCSNG
CDUSNone5NNo
17No
CDUS, GSUSNone12NoNGNo
Gynae exam, TV GSUS, CDUS, AngUAE15NoNGNo
GCUS, CDUShysteroscopy9NoLUSCSYes
GSUS, CDUSNone2NoNGNo
TA and TV GSUS and CDUSConservative6NoNVDYes
TA/TV, GSUS, CDUSConservative12NoLUSCSNo
48NVD
TA/TV GSUS CDUSConservative24NoLUSCSYes
TA/TV GSUS CDUSConservative24NoNo
TA/TV GSUS CDUSPrimulet4NoLUSCS (prior)Yes
TA/TV GSUS, CDUS, AngUAE9NoNVDYes
US, CDUS3–evacuation of RPOC 9–monitorNGNo'uncomplicated
TA/TV GSUS, CDUS, Duplex, Ang,15 UAENG01 LUSCS
4 NVD
9–CDUS14 UAENG1Two patients delivered 3 infants, one termination
14–Ang
TA/TV GSUS, CDUS, Ang17 UAE15.6 m06 pregnancies, 6 healthy, term babies
4–Palpation, CDUS, TV GSUS, 14–Ang' 1–Histo14 UAE 4 D&C 4 Hysterectomy1–5 y15 pts pregnant, 4 TA

UAE–uterine artery embolisation, BT–blood transfusion, SA–spontaneous abortion (miscarriage), Ang–angiography, D&C –dilation and curettage, Ix–investigations, OCP–oral contraceptive pill, NG–not given, ^–diagnosis of UAVM during a pregnancy, data not included in calculations *–patients went on to have multiple pregnancies post diagnosis of UAVM $–Patient did not go on to have a successful pregnancy, but did conceive post UAVM diagnosis

  37 in total

1.  Successful pregnancy with a full-term vaginal delivery one year after n-butyl cyanoacrylate embolization of a uterine arteriovenous malformation.

Authors:  Colleen C McCormick; Hyun S Kim
Journal:  Cardiovasc Intervent Radiol       Date:  2006 Jul-Aug       Impact factor: 2.740

Review 2.  Pelvic ultrasound in the postabortion and postpartum patient.

Authors:  Douglas L Brown
Journal:  Ultrasound Q       Date:  2005-03       Impact factor: 1.657

Review 3.  Color Doppler US in the evaluation of uterine vascular abnormalities.

Authors:  Pýnar Polat; Selami Suma; Mecit Kantarcý; Fatih Alper; Akýn Levent
Journal:  Radiographics       Date:  2002 Jan-Feb       Impact factor: 5.333

4.  Obstetric iatrogenic arterial injuries of the uterus: diagnosis with US and treatment with transcatheter arterial embolization.

Authors:  Jung Hyeok Kwon; Gi Sung Kim
Journal:  Radiographics       Date:  2002 Jan-Feb       Impact factor: 5.333

Review 5.  Uterine artery embolization: the role in obstetrics and gynecology.

Authors:  S Z Badawy; A Etman; M Singh; K Murphy; T Mayelli; M Philadelphia
Journal:  Clin Imaging       Date:  2001 Jul-Aug       Impact factor: 1.605

6.  Acquired uterine vascular malformations: radiological and clinical outcome after transcatheter embolotherapy.

Authors:  Geert Maleux; Dirk Timmerman; Sam Heye; Guy Wilms
Journal:  Eur Radiol       Date:  2005-06-24       Impact factor: 5.315

7.  Novel image-guided management of a uterine arteriovenous malformation.

Authors:  Stefan J Przybojewski; David J Sadler
Journal:  Cardiovasc Intervent Radiol       Date:  2010-08-06       Impact factor: 2.740

8.  Embolization of uterine arteriovenous malformation for treatment of menorrhagia.

Authors:  Sapna Patel; Sushma Potti; David Jaspan; Vani Dandolu
Journal:  Arch Gynecol Obstet       Date:  2008-07-30       Impact factor: 2.344

9.  Successful term pregnancy after selective embolization of a large postmolar uterine arteriovenous malformation.

Authors:  C-C Tsai; Y-F Cheng; C-C Changchien; H Lin
Journal:  Int J Gynecol Cancer       Date:  2006 Jan-Feb       Impact factor: 3.437

10.  Pregnancy following embolisation of uterine arteriovenous malformation--a case report.

Authors:  Y N Chia; C Yap; B S Tan
Journal:  Ann Acad Med Singapore       Date:  2003-09       Impact factor: 2.473

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  1 in total

1.  Severe hemorrhage due to acquired uterine arteriovenous malformation/fistula following first-trimester aspiration abortion: A case report.

Authors:  Kathryn E Sharpless; India I Pappas; Ethan M Dobrow; Matthew Moccia; Alison Bates; Michael G Pinette; Maureen Paul
Journal:  Case Rep Womens Health       Date:  2022-04-09
  1 in total

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