Material and Methods
Search Strategy
A literature search was performed in Medline, Cochrane, and Embase from 2003 to 2014.
The applied search heading included combinations of the following terms: “uterine
arteriovenous malformation,” “uterine AVM,” “uterus and malformation,” “uterine fistula,”
“uterine shunt,” “hysterectomy,” “resection,” “surgical,” and “embolization” limited
to clinical studies published in the English language. Titles and abstracts were screened
to identify relevant articles. Referred and related articles were checked. Articles
were selected following the selection criteria below and evaluated by two of the authors
(D. J. Y., J. D. D.) using a scoring list. For this type of study, formal consent
is not required.
Selection Criteria and Data Extraction
All clinical studies on acquired uterine AVM were included for further evaluation.
Acquired AVM was defined as a uterine AVM pertaining to or diagnosed following trauma,
surgical intervention, or in the setting of a preexisting pathologic uterine process.
Included articles described the uterine AVM as acquired and included a description
of the underlying pathology. Articles were excluded if they were review articles or
animal studies, or did not describe the specifics of the technical approach as below.
All included studies were evaluated for study quality characteristics by two reviewers
and included: (1) patient characteristics (number of patients, age, time of diagnosis,
method of diagnosis, inciting cause of the acquired uterine AVM); (2) indication for
embolization; (3) embolization technique (unilateral or bilateral) and embolic material
utilized; (4) technical outcome; (5) follow-up (clinical success rate, postprocedural
complications and morbidity, postprocedural imaging); (6) requirement for additional
embolization procedure, medical management, or surgery. Articles were valid and used
for data extraction if the above-mentioned points were clearly described.
Results
The broad initial search using the search heading “uterine arteriovenous malformation”
resulted in 304 publications. Primary survey of the abstracts and articles excluded
224 articles dealing with subjects other than transcatheter embolization, animal studies,
reviews or articles in a non-English language. After critical evaluation of the remaining
full text articles for acquired uterine AVMs, 40 articles remained for final inclusion
meeting the minimum requirements above and comprised of 39 case reports[2]
[3]
[4]
[5]
[6]
[7]
[8]
[9]
[10]
[11]
[12]
[13]
[14]
[15]
[16]
[17]
[18]
[19]
[20]
[21]
[22]
[23]
[24]
[25]
[26]
[27]
[28]
[29]
[30]
[31]
[32]
[33]
[34]
[35]
[36]
[37]
[38]
[39]
[40] and one retrospective study.[41] The cumulative evaluated population comprised of 54 women with a mean age of 33.5
years. The underlying pathology is summarized in [Table 1].
Table 1
Associated clinical history for reported cases of acquired uterine AVM
|
Associated clinical history
|
Number (%)
|
|
D&C
|
34 (62)
|
|
C-section
|
14 (26)
|
|
Uterine instrumentation procedures (hysteroscopy, placental delivery, and IUD placement)
|
2 (4)
|
|
Myomectomy
|
2 (4)
|
|
GTT
|
2 (4)
|
|
Total
|
54
|
Abbreviations: AVM, arteriovenous malformation; D&C, dilation and curettage; GTT,
Gestational trophoblastic tumor; IUD, intrauterine device.
Pathophysiology of Uterine Arteriovenous Malformations
Based on the vascular anomaly classification proposed by Mulliken and Glowaki, AVMs
can be defined as a vascular structural anomaly involving abnormal communication between
arteries and veins that bypass the capillary system.[42] AVMs can be further categorized as high-flow vascular malformations as typified
by a high-pressure gradient across the arterial and venous system that enables a high
vascular flow through the nidus, the intervening network of vessels communicating
the arteries to the veins. Alternatively, a direct communication may exist in the
absence of a nidus representing a fistulous connection of the arteries and venous
structures. Though AVMs involving the uterus are rare, if present, they can be a serious
cause of recurrent and intermittent menorrhagia.
Uterine AVMs are divided into congenital and acquired AVMs. Congenital AVMs result
from a defect in the differentiation of the primitive capillary plexus during fetal
angiogenesis.[43]
[44]
[45]
[46] In contradistinction, acquired AVMs are vascular abnormalities usually present after
trauma, surgical intervention, or in the setting of a preexisting pathologic uterine
process. An acquired uterine AVM is characterized by a single arteriovenous communication
between the branches of the uterine artery and the myometrial venous plexus. Indeed,
terms, including “arteriovenous fistula,” “traumatic uterine arteriovenous malformation,”
and “arteriovenous shunt” are interchangeably used in the literature, despite their
differences, to describe such acquired pathology which may be difficult to differentiate.
To follow those descriptions in the literature and for the purposes of this review,
these terms are also collectively referred to as acquired uterine AVM although the
exact underlying pathophysiology is not well understood.[8] Although the term malformation may suggest a congenital etiology, acquired uterine
AVMs develop following an inciting event, differentiating them from their congenital
counterpart. For instance, packing and clamping for hemostatic control during surgery
can cause shunting of blood from the capillary plexus to the less resistant venous
system possibly resulting in fistula formation after uterine procedures.[10] Case reports have described acquired AVM formation following uterine dilation and
curettage (D&C), cesarean section, and myomectomy.[6]
[8] Pathologic processes such as infection, trophoblastic disease, and malignancies
involving the uterus have also been described as associated with acquired AVM.[47]
The association of pregnancy and worsening symptoms of acquired uterine AVM formation
suggests a hormonal mechanism. Pregnancy and associated hormonal changes, such as
elevated human chorionic gonadotropin (hCG),[48] may play a role in the proliferation of otherwise latent AVMs through an unclear
mechanism.[7]
[47] Similarly, women undergoing fertility treatments may be at higher risk secondary
to elevated estrogen level, causing endothelial proliferation and differentiation
of the endometrium.[48] However, menorrhagia after pregnancy may also be a representation of retained product
of conceptions or nonobliteration and subinvolution of the blood vessels of the placental
bed rather than secondary to AVM formation.[44]
[49] These former entities share similar radiologic findings with acquired AVMs, which
can make differentiation of these separate pathologic processes difficult.[44] Ultimately, increased efforts to identify those mechanisms underlying the formation
of acquired uterine AVMs may allow for the identification of those patients at risk
for their development and prompt early and close follow-up to avoid the associated
complications.
Clinical Presentation
Acquired uterine AVMs are typically identified in symptomatic, multiparous women of
childbearing age. A systematic review of the demographics of iatrogenic, acquired
AVMs by Peitsidis et al revealed the mean age of women diagnosed with a uterine AVM
was 30 years.[50] Acquired uterine AVM rarely affects nulliparous women without a history of uterine
trauma secondary to gynecological procedures.[47] The most common presenting symptoms of an acquired uterine AVM are menorrhagia and
metrorrhagia. Bleeding is often intermittent and torrential.[4] This is secondary to the high vascular flow across the involved lesion due to the
differential pressure gradient across the arterial and venous systems. These patients
may also present with anemia and hypotension, secondary to acute blood loss. Peitsidis
et al recently identified that approximately 50% of patients with acquired uterine
AVM required blood transfusion secondary to the associated anemia.[50] Vague pelvic discomfort, urinary symptoms, including polyuria and incontinence,
and dyspareunia are common complaints.[4] Congestive heart failure secondary to the shunting of blood to the venous system
is possible but is rare.[51] A history of recurrent spontaneous abortion may also place a patient at higher risk
for acquired uterine AVM formation, possibly due to the increased vascularization
and resultant physical alteration of the embryo's implantation site.[33] Despite these common presenting symptoms, patients may alternatively remain asymptomatic
despite the presence of a uterine AVM. Asymptomatic patients may later develop symptoms
following uterine trauma or secondary to hormonal changes related to pregnancy or
the menstrual cycle.[52]
Diagnosis
The differential diagnosis for a woman of childbearing age presenting with menorrhagia
and metrorrhagia is broad.[53] Although rare, acquired uterine AVM should be considered in patients with appropriate
history and presenting symptoms. Notably, the typical treatment options for uterine
bleeding, such as D&C, can cause uterine trauma and paradoxically worsen the bleeding
in the presence of an acquired AVM. D&C is therefore contraindicated in acquired uterine
AVM or those patients with suspected acquired AVM.[4] If there is increased bleeding during a D&C performed for abnormal uterine bleeding,
then a uterine AVM should be suspected and the appropriate precautions taken for the
possibility of ongoing severe hemorrhage.
Historically, acquired uterine AVM was diagnosed by pathology after hysterectomy.[44] Recently, less invasive imaging studies have been utilized for diagnostic purposes
to guide therapeutic options. Transvaginal ultrasound is the initial imaging study
of choice for abnormal uterine bleeding. As a definitive diagnosis based on grayscale
ultrasound imaging is difficult alone, Doppler imaging is imperative to the diagnosis.
The presence of a tubular, hypoechogenic structure in the myometrium by grayscale
ultrasound imaging, although common, is not specific for uterine AVM. The identification
of uterine high velocity blood flow with low impedance by Doppler ultrasound is highly
suggestive for a uterine AVM[44]
[54] ([Fig. 1a]). As mentioned earlier, subinvolution of the placental bed and adenomyosis in the
setting of menorrhagia also can have similar ultrasound findings such as hypervascularity
and turbulent flow. There are no firm criteria to differentiate between an AVM and
the subinvolution of the placenta by ultrasound.[44] This raises a concern for the overdiagnosis of uterine AVM. Magnetic resonance imaging
(MRI) is thus recommended for the evaluation beyond ultrasound for uterine AVM when
indicated, particularly in cases when the acoustic windows are limited by body habitus
or technique. MRI findings include serpiginous signal voids in the uterus and enhancement
of the signal voids on rapid data acquisition during infusion of contrast.[54]
[55]
[56] MRI provides better tissue contrast and helps delineate the surrounding pelvic organ
involvement. Acquired AVM primarily involves the myometrium while retained products
of conception primarily involve the endometrium.[56] The diagnosis can be confirmed when these imaging findings are coupled with maternal
serum hCG, which has a slower decline in retained products of conception. Computed
tomography (CT) can assess the degree of involvement of the surrounding visceral structures[57]; however, utilizes ionizing radiation, which should be avoided in women of childbearing
age and does not contribute additional information beyond that garnered by MRI. Characteristic
CT findings include the presence of a soft-tissue density mass with enhancement pattern
resembling adjacent vessels.[58] Angiography should be offered in consideration for a possible therapeutic option
following diagnostic confirmation. The typical findings of a uterine AVM by angiography
include high arterial flow with early venous filling ([Fig. 1c, d]). A single direct fistulous communication to the venous structures may be identified.
This finding is more common in acquired AVM ([Fig. 1d]) than in congenital AVM, where contrast filling of a vascular plexus or nidus is
more commonly seen.[44] In this representative case ([Fig. 1e]), a novel treatment approach to uterine AVMs was utilized in which the malformation
was embolized using a nonadhesive liquid embolic agent, Onyx (ev3 Endovascular Inc.,
Plymouth, MN), with complete resolution of the uterine AVM on follow-up MRI ([Fig. 1f]).
Fig. 1 Unilateral Onyx (ev3 Endovascular Inc., Plymouth, MN) embolization, a type of nonadhesive
liquid embolic agent, for an acquired uterine AVM. A 30-year-old G1P1001 presented
with vaginal bleeding 9 days following D&C for retained products of conception. (A)
Color Doppler ultrasound of the uterus in sagittal plane reveals a heterogeneous,
hyperechoic region within the anterior fundal myometrium extending to the endometrium
with an increased vascularity. (B) DSA of the aorta with contrast demonstrates increased
vascularity arising from the left uterine artery and a normal appearing right uterine
artery. (C) Selective catheter angiography of the left internal iliac artery with
contrast confirms an acquired uterine AVM arising from the uterine artery with arteriovenous
shunting. (D) Early venous filling is also noted on delayed imaging. (E) Post-Onyx
embolization angiography reveals total occlusion of the AVM. (F) Representative coronal
images from follow-up MRI showing preservation of uterine perfusion, absence of a
vascular malformation, and associated artifact from the Onyx embolic agent. AVM, arteriovenous
malformation; D&C, dilation and curettage; DSA, Digital subtraction angiography; MRI,
magnetic resonance imaging.
Treatment
Transcatheter Embolization
Historically, treatment for symptomatic, acquired uterine AVM required hysterectomy[2]; however, since its description in the late 1980s,[59] TCE has provided an alternative and less invasive treatment option for patients
wishing to preserve fertility. Review of articles on embolization technique utilized
in the treatment of acquired uterine AVMs was performed using the criteria described
above. The results of the cumulative 54 patients reviewed from 40 studies as reported
as having acquired uterine AVMs are summarized in [Tables 1]
[2]
[3].
Table 2
Unilateral versus bilateral approach for uterine AVM
|
Laterality
|
Number (N)
|
Requiring repeat embolization or medical treatment
|
Repeat embolization or medical treatment resulting in the resolution of symptoms
|
Requiring hysterectomy or other surgeries
|
References
|
|
Unilateral
|
22
|
4 (1 medical treatment, 3 repeat) (18.2%)
|
4
|
2 (9.5%)
|
[2]
[3]
[7]
[8]
[9]
[10]
[14]
[15]
[16]
[17]
[18]
[19]
[22]
[23]
[29]
[31]
[33]
[35]
[41]
|
|
Bilateral
|
32
|
14 (4 medical treatment, 10 repeat) (43.8%)
|
9
|
6 (18.8%)
|
[4]
[5]
[6]
[9]
[11]
[12]
[13]
[20]
[21]
[24]
[25]
[26]
[27]
[28]
[30]
[32]
[34]
[36]
[37]
[38]
[39]
[40]
[41]
|
|
Total
|
54
|
18
|
13
|
8
|
–
|
Abbreviation: AVM, arteriovenous malformation.
Table 3
Embolic agents for acquired uterine AVMs
|
Embolic agents used
|
Number (N)
|
Requiring repeat embolization or medical treatment
|
Repeat embolization or medical treatment resulting in the resolution of symptoms
|
Hysterectomy or other surgeries
|
References
|
|
Glue
|
7
|
2 (both repeated with glue)
|
2
|
1 (no repeat or medical treatment)
|
[6]
[27]
[31]
[41]
|
|
Gelfoam
|
7
|
2 (repeat with coil and embosphere, danazol)
|
1 (danazol-controlled bleeding)
|
1 (after repeat)
|
[7]
[9]
[12]
[25]
[32]
[38]
[41]
|
|
Microsphere
|
5
|
2 (implanon therapy, repeat with microspheres)
|
1
|
1 (uterine AVM resection after repeat)
|
[7]
[16]
[17]
[40]
|
|
Coils
|
6
|
1 (repeat with glue coil)
|
1
|
2 (no medical treatment or repeats)
|
[2]
[8]
[10]
[18]
[20]
[21]
|
|
PVA
|
6
|
0
|
0
|
0
|
[14]
[23]
[28]
[34]
[36]
[41]
|
|
Glue, Gelfoam
|
2
|
2 repeat with glue/Gelfoam
|
2
|
0
|
[41]
|
|
Gelfoam, NBCA
|
2
|
1 (progesterone)
|
1
|
0
|
[4]
[29]
|
|
Glue, coil
|
2
|
1 (repeat with glue coil)
|
1
|
0
|
[4]
[41]
|
|
NBCA, coil
|
1
|
0
|
0
|
0
|
[30]
|
|
PVA, Gelfoam
|
2
|
2 (OCP/tranexamic acid, methotrexate)
|
1 (controlled by methotrexate)
|
1 (due to continuous bleeding after OCP)
|
[11]
[24]
|
|
Coil, Gelfoam
|
3
|
0
|
0
|
0
|
[13]
[26]
[39]
|
|
NBCA, microsphere
|
1
|
0
|
0
|
0
|
[19]
|
|
PVA, microsphere
|
2
|
1 (Onyx, embosphere)
|
0
|
1 (after repeat)
|
[15]
[22]
|
|
Gelfoam, microsphere
|
2
|
0
|
0
|
0
|
[33]
[35]
|
|
PVA, coil
|
1
|
1 (repeat with coil)
|
1
|
0
|
[37]
|
|
PVA, glue
|
3
|
2 (both repeat with Onyx and glue)
|
1
|
1 (after repeat)
|
[41]
|
|
Gelfoam, NBCA, coil
|
1
|
1 (repeat with same agent)
|
1
|
0
|
[3]
|
|
Onyx, NBCA, Gelfoam
|
1
|
0
|
0
|
0
|
[5]
|
|
Total
|
54
|
18
|
13
|
8
|
|
Abbreviations: AVM, arteriovenous malformation; NBCA, N-butyl cyanoacrylate; OCP, oral contraceptive pills; PVA, polyvinyl alcohol.
Note: Gelfoam (Pharmacia and Upjohn Company, Kalamazoo, MI), Onyx (ev3 Endovascular
Inc., Plymouth, MN).
The mean age of the 54 patients meeting review criteria was 33.5 ± 10.2 years ([Table 1]). Of 54 patients, 50 (93%) of them had a history of uterine procedures, such as
D&C, cesarean section, or had a history of gestational trophoblastic tumor ([Table 1]). Four patients (7.4%) did not have such history; however, all of them had a history
of spontaneous abortion without D&C.[7]
[18]
[23] Out of the 54 patients 33 (61%) had symptoms controlled following the initial embolization.
Although congenital AVMs, particularly if large, are usually approached in a methodical,
stepwise manner to embolization, acquired uterine AVMs are usually encountered in
the setting of menorrhagia and approached toward single-setting symptomatic hemostatic
control. Nevertheless, acquired uterine AVMs may require repeat embolization for treatment
and this should not be considered as a failure of embolization but rather as a requirement
for additional treatments. Of the 21 patients who continued to be symptomatic following
the initial embolization, 13 (62%) underwent repeat embolizations[3]
[6]
[9]
[15]
[20]
[23]
[40]
[41] (Ghai et al included 7 cases), 5 (24%) underwent medical treatments with agents
such as danazol, progesterone, combination oral contraceptive pills (OCP), implanon
therapy, or methotrexate,[4]
[7]
[11]
[24]
[32] 2 (10%) underwent hysterectomy,[2]
[21] and 1 (5%) underwent laparoscopic occlusion of the internal iliac arteries.[27] Of the 13 patients who underwent repeat embolization, 9 cases (69%) resulted in
the resolution of the symptoms. Two patients who continued to bleed after the repeat
embolization therapy underwent hysterectomy,[15]
[41] one patient underwent partial resection of the uterus,[9] and one patient underwent laparoscopic resection of the AVM.[40] Of the five patients who underwent concurrent medical therapy, four resulted in
the resolution of the symptoms.[4]
[7]
[24]
[32] The one patient who failed the combination OCP therapy after initial embolization
underwent hysterectomy.[11] Taking into consideration both initial and follow-up embolization procedures, TCE
had a primary success rate of 61% and secondary success rate of 91% after repeated
embolization.
Based on the literature search, there are no definitive treatment guidelines for patients
who fail initial embolization. Further, there have been no studies completed comparing
the effectiveness of repeat embolization versus medical therapy versus hysterectomy
for persistent bleeding after initial embolization. In total, TCE and combination
of medical therapy resulted in the eventual resolution of symptoms in 46 (85%) out
of 54 patients without more invasive surgical procedures.
The use of a unilateral or bilateral approach for TCE must be determined in the treatment
of a uterine AVM. Of the 54 patients reviewed, 22 (41%) underwent unilateral embolization
and the other 32 (59%) underwent bilateral embolization ([Table 2]). The decision on laterality should be based on the arterial supply to the AVM determined
by the angiographic appearance. After the dominant side of the artery supplying the
AVM was embolized, the decision to embolize the contralateral side was largely dependent
on the clinical scenario and the preference of the interventional radiologist. Of
the 22 patients who underwent unilateral embolization, 1 required medical treatment
following embolization, 3 required repeat embolization, and 2 required eventual hysterectomy
([Table 2]).[2]
[7]
[15] Of the 32 of 54 reviewed patients who underwent bilateral embolization for acquired
uterine AVM ([Table 2]), 4 required medical therapy following embolization, 10 required repeat embolization,
and 6 required eventual surgery secondary to persistent bleeding.[9]
[11]
[21]
[37]
[38]
[40]
[41] Although uterine AVM size was not reported, the higher rate of repeat embolization
for the bilateral approach TCE cases may be speculated to reflect larger or more deeply
involved lesions. The ovarian artery was embolized using gelatin sponge with symptomatic
control at the time of initial TCE for two cases.[4] No other cases described embolization of parasitized arteries. No controlled studies
have been performed to evaluate the effectiveness of a unilateral versus bilateral
treatment approach. Further, given the differences in embolic agents, AVM size and
history, and clinical symptoms, no direct comparison can be made in these cases in
regards to a unilateral or bilateral approach.
A variety of embolic agents and combination of embolic agents were used for treatment
in the reviewed cases, and the choices of the embolic agents were largely based on
the preference of the interventional radiologists. The embolic agents used in the
literature are summarized in [Table 3]. Based on this literature search there has been no study comparing the efficacy
of each embolic agent, or combinations of agents. Glue (seven cases [13%] [Ghai et
al included four cases]),[6]
[27]
[31]
[41] Gelfoam (Pharmacia and Upjohn Company, Kalamazoo, MI) (seven cases [13%]),[7]
[9]
[12]
[25]
[32]
[38]
[41] coils (six cases [11%]),[2]
[8]
[10]
[18]
[20]
[21] polyvinyl alcohol (PVA) (six cases [11%]),[14]
[23]
[28]
[34]
[36]
[41] microspheres (five cases [9%] (Halperin et al included two cases)][7]
[16]
[17]
[40] were the most commonly used embolic agents as single agents. There were 14 other
combinations of embolic agents used in the literature ([Table 3]). Although oftentimes utilized for the treatment of congenital AVMs, alcohol was
not described in the included articles for the treatment of the acquired uterine AVM.
Despite the numerous combinations and options in embolic agents utilized, there were
no significant differences in the necessity for repeat embolization amongst these
techniques, given the limitations in sample size and differences in the laterality
of approach.
The literature available for review is limited to the treatment of acquired uterine
AVMs given its rarity. However, the clinical significance of this diagnosis underscores
the importance of understanding the approaches and techniques available for its treatment.
Our inclusion criteria excluded studies that did not clearly describe embolic agents,
the laterality of approach, and therapeutic outcomes associated with each patient
limiting the available literature to low-level evidence including case reports and
retrospective studies. The follow-up period in each case report or retrospective study
greatly varied from weeks to years, which may have overstated the therapeutic success
rate. Finally, some of the studies included failed to clearly distinguish acquired
uterine AVM from other possible pathologic entities such as retained products of conception
or involution of placenta. This is not surprising given the inability in many cases
for pathologic confirmation and the radiologic similarities on diagnostic imaging
studies. However, from a minimally invasive treatment perspective, this may not be
critical as the approach may be similar for these etiologies although possibly different
for a congenital vascular lesion.
Surgical Approaches
Currently, hysterectomy is indicated only for those women who do not desire fertility
preservation and have limited access to medical facilities.[11] The advancement of transcatheter embolization described above and the utilization
of medical therapy provide options to avoid more invasive surgical approaches. Given
the success of these treatment modalities, the literature is dedicated more toward
the advancement of these techniques rather than surgical approaches and hysterectomy
for treatment of acquired AVMs. However, hysterectomy is an appropriate option when
conservative measures have failed to prevent a life-threatening hemorrhage. Both congenital
and acquired AVMs have a high propensity to bleed given the inability of these arteriovenous
connections to withstand high flow and elevated pressure, so appropriate consideration
must be given before surgical intervention.[60] Given the acuity of clinical situations that necessitate surgical intervention and
the distorted uterine tissue and anatomy created by an AVM, hysterectomy should be
performed by those skilled in radical pelvic surgical techniques.[60]
[61]
Minimally invasive surgical techniques have also been performed for the treatment
of uterine AVMs.[62]
[63]
[64] Laparoscopic occlusion of the internal iliac arteries was successfully performed
using nonresorbable clips for an acquired uterine AVM that had persistent bleeding
6 weeks following two uterine artery embolization procedures.[27] Additionally, surgical ligation of the uterine arteries after TCE has been reported[2]
[62] as well as when coupled with laparoscopic myometrial lesion resection.[64] Unilateral or bilateral laparoscopic bipolar coagulation of the uterine arteries
has also been performed successfully for acquired uterine AVM.[63]
[64] These procedures were most commonly performed for persistent bleeding despite initial
or repeat TCE. The role of these minimally invasive surgical techniques as a primary
or secondary treatment for uterine AVM as well as in fertility following such surgeries
requires further investigation.
Postprocedural Management
Among 54 TCE cases reviewed, there were no major complications. Six developed pelvic
pain or cramping, which were the most common side effects reported following TCE.
These were either self-limited or controlled by opioids or acetaminophen.[4]
[7]
[23]
[35]
[36]
[38] There was also one patient with a postprocedural fever, a characteristic of postembolization
syndrome, which was self-limited.[35] In terms of postembolization syndrome, a 2-week course of oral nonsteroidal anti-inflammatory
should be considered following uterine artery embolization. Other reported complications
of TCE include nausea and leukocytosis as well as those complications related to standard
angiographic technique, such as puncture site hematoma, iatrogenic vessel dissection,
and contrast-induced nephrotoxicity .[65] Successful subsequent pregnancy and delivery following TCE has been described in
14 cases (Ghai et al included 4 cases).[4]
[6]
[16]
[19]
[20]
[23]
[30]
[31]
[33]
[36]
[41] The effect of TCE on infertility is difficult to ascertain as the literature is
biased toward those studies describing cases of a successful pregnancy following embolization.
To note, TCE may be associated with an increased risk for placental abnormalities
in subsequent gestations, specifically placenta accreta,[66]
[67] and an increased awareness of this risk should be considered in future pregnancies
following a successful embolization.
Following hysterectomy, routine postoperative care should include careful attention
to pain control and bladder function due to adjacent radical dissection of the uterus,
cervix, and parametrium. Hemostasis and coagulation will likely improve after removal
of the bleeding source and abnormal tissue[68]; however, tortuous, dilated ovarian, uterine, and iliac vessels can remain a source
for continued bleeding postoperatively despite ligation. Long-term follow-up is necessary
to ensure continued hemostasis and to evaluate recurrence of the AVM.[2] Embolization, used as an adjunct to hysterectomy, surgical resection of AVM, or
vascular ligation has been described.[2]
[61] In general, hysterectomy requires intensive management of pain and, for the majority
of the cases, at least 1 day of hospitalization. Routine postoperative care, including
monitoring of the vitals and urinary output is required. Prophylaxis against the occurrence
of major thrombotic events is important. Full recovery can be expected in approximately
4 to 8 weeks following hysterectomy for an acquired AVM.
As uterine AVM remains a rare entity, no definitive guidelines are recommended for
the treatment or follow-up for asymptomatic uterine AVM. In our practice, acquired
uterine AVM patients are followed in conjunction between the patient's gynecologist
and interventionalist. Repeat imaging is completed in our patients to confirm obliteration
after treatment or when clinically indicated by persistent or worsening symptoms to
evaluate for additional treatment. Incidentally discovered, asymptomatic uterine AVMs
are less described in the literature; however, are followed clinically with a risk
to benefit assessment for each patient individually to determine the necessity or
timing of treatment.
