AJR 2005; 184:555-559
© American Roentgen Ray Society
MRI of Uterine Necrosis After Uterine Artery Embolization for Treatment of Uterine Leiomyomata
Drew A. Torigian1,
Evan S. Siegelman1,
Kyla P. Terhune2,
Samantha F. Butts3,
Luis Blasco3 and
Richard D. Shlansky-Goldberg1
1 Department of Radiology, Hospital of the University of Pennsylvania, 3400
Spruce St., Philadelphia, PA 19104–4283.
2 Department of Pathology and Laboratory Medicine, University of Pennsylvania
School of Medicine, Philadelphia, PA 19104–4283.
3 Department of Obstetrics and Gynecology, Hospital of the University of
Pennsylvania, Philadelphia, PA 19104.
Received April 19, 2004;
accepted after revision July 21, 2004.
Address correspondence to D. A. Torigian
(Drew.Torigian{at}uphs.upenn.edu).
Introduction
We report the clinical, pathologic, and MRI findings of a woman with
symptomatic uterine leiomyomata who underwent therapeutic uterine artery
embolization, which was complicated by uterine necrosis requiring
hysterectomy, as depicted on MRI.
Case Report
A 47-year-old premenopausal woman with a remote history of prior cesarean
delivery (at least 10 years ago) and a recent history of menorrhagia for
several months' duration presented to the department of radiology for pelvic
MRI. MRI of the pelvis with a standard phased array torso coil was performed
on a 1.5 Tesla magnet (Signa, GE Healthcare) at baseline using axial
T1-weighted fast spin-echo images; axial, sagittal, and coronal T2-weighted
fast spin-echo images (fat-suppressed in the coronal plane); axial
fat-suppressed T1-weighted out-of-phase spoiled gradient-echo images; sagittal
pre- and dynamically enhanced post–gadolinium fat-suppressed 3D
T1-weighted out-of-phase spoiled gradient-echo MR angiographic images; and
axial and sagittal delayed post–gadolinium fat-suppressed T1-weighted
out-of-phase spoiled gradient-echo images. This MRI of the pelvis at baseline
showed enlargement of the uterus (13.6 x 9.6 x 18.0 cm) due to the
presence of multiple (about 30–40) 0.7–5.7 cm predominantly
intramural leiomyomata with intermediate signal intensity on both T1-weighted
images (Fig. 1A) and
T2-weighted images (Fig. 1B)
relative to skeletal muscle, several of which showed a submucosal component.
Several leiomyomata were subserosal in location, but none were pedunculated or
intracavitary in location. None of the leiomyomata revealed T1-weighted
hyperintensity or had an intracavitary location. All except two leiomyomata
showed enhancement on gadolinium-enhanced T1-weighted images
(Fig. 1C). The normal
surrounding uterine myometrium showed intermediate signal intensity on
T1-weighted images and intermediate to slightly high signal intensity on
T2-weighted images relative to skeletal muscle, and diffuse enhancement (Fig.
1A,
1B,
1C). Single uterine arteries
were present bilaterally on the sagittal MR angiographic images (matrix, 320
x 160) without visualization of ovarian arterial collateral supply. The
patient's leiomyomata were considered to be contributing to her menorrhagia,
and she elected to undergo uterine artery embolization as a minimally invasive
treatment.
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Fig. 1A. —47-year-old woman with symptomatic uterine leiomyomata who
presented for pelvic MRI. Axial T1-weighted fat-suppressed out-of-phase
gradient-echo image (TR/TE/FA, 160/1.5/90) obtained through uterus shows
enlarged uterus with intermediate signal intensity of viable myometrium (M)
and leiomyoma (F) relative to skeletal muscle.
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Fig. 1B. —47-year-old woman with symptomatic uterine leiomyomata who
presented for pelvic MRI. Sagittal T2-weighted fast spin-echo image (TR/TE,
5,700/81) obtained through midline of uterus shows intermediate signal
intensity of leiomyomata (F) and intermediate to slightly high signal
intensity of surrounding myometrium relative to skeletal muscle.
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Fig. 1C. —47-year-old woman with symptomatic uterine leiomyomata who
presented for pelvic MRI. Axial delayed gadolinium-enhanced fat-suppressed
T1-weighted out-of-phase gradient-echo image (TR/TE/FA, 180/1.5/90) shows
diffuse enhancement of viable myometrium (M) and leiomyoma (F).
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Two weeks later, the patient underwent bilateral uterine artery
embolization in standard fashion using 355- to 500-µm polyvinyl alcohol
(PVA) particles (Boston Scientific; Target Therapeutics) to the point of
stasis of blood flow within the visualized single uterine arteries as per
Spies et al. [1]. No immediate
postprocedural complications were noted, and the patient was subsequently
discharged on the same day.
Four days after undergoing the procedure, the patient presented to the
emergency department with 1 day of fever to 103°F (39°C), acute lower
abdominal pain, and nausea and vomiting. Physical examination revealed an
irregularly enlarged diffusely tender uterus, along with mild vaginal bleeding
and a foul-smelling vaginal discharge. The cervix was normal in appearance
with a closed os, the adnexa were nonpalpable, and the remainder of the
physical examination was unremarkable. Laboratory analysis revealed moderate
leukocytosis and anemia. Blood cultures were obtained that never became
positive; uterine cultures were not obtained. At this time, the differential
diagnosis included postembolization syndrome and endometritis, and the patient
was empirically placed on triple antibiotic therapy (ampicillin, gentamicin,
and clindamycin) along with pain and antiemetic medications without clinical
improvement.
Repeat pelvic MRI on the same day showed no change in overall uterine
volume or in the size or number of uterine leiomyomata. All the uterine
leiomyomata now showed high signal intensity on T1-weighted images
(Fig. 2A) and intermediate to
slightly high signal intensity on T2-weighted images
(Fig. 2B) relative to skeletal
muscle and did not enhance (Figs.
2C and
2D), in keeping with necrosis.
However, most of the surrounding uterine myometrium now showed intermediate to
high signal intensity on T1-weighted images
(Fig. 2A), high signal
intensity on T2-weighted images (Fig.
2B), and lack of enhancement. Residual areas of enhancing
subserosal myometrium were sparsely present, measuring approximately
0.1–1 cm in thickness. The endometrial stripe did not enhance in keeping
with necrosis. A diagnosis of near-total uterine necrosis was made, and the
patient subsequently underwent a total abdominal hysterectomy.
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Fig. 2A. —47-year-old woman (same woman as in Fig.
1A,
1B,
1C) 4 days after uterine artery
embolization for symptomatic uterine leiomyomata who presented with new fever,
lower abdominal pain, nausea, vomiting, uterine tenderness, foul-smelling
vaginal discharge, and leukocytosis. Axial T1-weighted fat-suppressed
out-of-phase gradient-echo image (TR/TE/FA, 195/1.5/90) obtained through
uterus shows high signal intensity of uterine leiomyoma (F) relative to
skeletal muscle due to coagulative necrosis and intermediate to high signal
intensity of surrounding necrotic uterine myometrium.
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Fig. 2B. —47-year-old woman (same woman as in Fig.
1A,
1B,
1C) 4 days after uterine artery
embolization for symptomatic uterine leiomyomata who presented with new fever,
lower abdominal pain, nausea, vomiting, uterine tenderness, foul-smelling
vaginal discharge, and leukocytosis. Sagittal T2-weighted fast spin-echo image
(TR/TE, 6,000/85) obtained through midline of uterus shows several
intermediate to slightly high-signal-intensity lesions due to uterine
leiomyomata (F) and extensive high signal intensity of surrounding myometrium
secondary to coagulative necrosis relative to skeletal muscle. Peripheral
scattered areas and thin subserosal rim of intermediate to slightly
high-signal-intensity viable myometrium (arrow) are seen. Endometrium
is poorly visualized because of distortion by leiomyomata.
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Fig. 2C. —47-year-old woman (same woman as in Fig.
1A,
1B,
1C) 4 days after uterine artery
embolization for symptomatic uterine leiomyomata who presented with new fever,
lower abdominal pain, nausea, vomiting, uterine tenderness, foul-smelling
vaginal discharge, and leukocytosis. Axial (C) and sagittal plane
(D) delayed gadolinium-enhanced fat-suppressed T1-weighted out-of-phase
gradient-echo images (TR/TE/FA, 195/160/90 and 160/1.5/90, respectively) show
lack of enhancement of uterine leiomyomata, endometrium, and myometrium in
keeping with necrosis (N), with enhancement of only peripheral scattered areas
and subserosal rim of viable myometrium (arrow).
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Fig. 2D. —47-year-old woman (same woman as in Fig.
1A,
1B,
1C) 4 days after uterine artery
embolization for symptomatic uterine leiomyomata who presented with new fever,
lower abdominal pain, nausea, vomiting, uterine tenderness, foul-smelling
vaginal discharge, and leukocytosis. Axial (C) and sagittal plane
(D) delayed gadolinium-enhanced fat-suppressed T1-weighted out-of-phase
gradient-echo images (TR/TE/FA, 195/160/90 and 160/1.5/90, respectively) show
lack of enhancement of uterine leiomyomata, endometrium, and myometrium in
keeping with necrosis (N), with enhancement of only peripheral scattered areas
and subserosal rim of viable myometrium (arrow).
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At laparotomy, an 18-week-sized leiomyomatous uterus was present that had
multiple areas of pallor and duskiness and areas of bogginess. Grossly, the
ovaries appeared normal.
On pathologic examination, the gross specimen had the appearance of
multiple uterine leiomyomata without hemorrhage
(Fig. 3A). Histologic
examination showed extensive coagulative necrosis of multiple uterine
leiomyomata and of most of the surrounding myometrium with a subcentimeter rim
of viable subserosal myometrium (Fig.
3B). Necrosis of the endometrium was also present, along with
partial or complete occlusion of multiple uterine arterial branches by PVA
particles admixed with fibrin. These findings were interpreted as ischemic
necrosis related to recent uterine artery embolization.
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Fig. 3A. —Gross and histopathologic findings of excised uterus of
47-year-old woman (same woman as in Fig.
1A,
1B,
1C). Photograph of sectioned
gross specimen shows multiple masses in enlarged uterus due to uterine
leiomyomata.
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Fig. 3B. —Gross and histopathologic findings of excised uterus of
47-year-old woman (same woman as in Fig.
1A,
1B,
1C). Photomicrograph of
histologic specimen of uterine myometrium shows myometrial coagulative
necrosis (N) with "ghosts" of dead myometrial cells adjacent to
viable myometrial cells (V) that have visible elongated nuclei. (H and E,
x20)
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Discussion
Transcatheter embolization of the uterine arteries has been used over the
past 8 years as a minimally invasive means of managing symptomatic uterine
leiomyomata with preservation of the uterus
[2]. Major complications after
uterine artery embolization, as per strict (SIR class D) criteria occur in
approximately 1.25% of cases as shown in a series of 400 patients by Spies et
al. [1], and the rate of
hysterectomy following uterine artery embolization ranges between
0.25–1.6%, with causes attributed to infection, pain, and bleeding
[3,
4]. However, uterine necrosis
is a rare complication of uterine artery embolization, with fewer than 10
cases reported in the literature, which necessitates treatment with
antibiotics and hysterectomy to prevent bacteremia, sepsis, and death
[4–11].
MRI may be used to confirm a diagnosis of uterine necrosis after uterine
artery embolization so that early treatment may be implemented. To our
knowledge, this is the first report of the MRI findings of uterine necrosis
after therapeutic uterine artery embolization for symptomatic uterine
leiomyomata.
Godfrey and Zbella [5]
reported on a patient with uterine necrosis occurring approximately 2–3
months after uterine artery embolization was performed for symptomatic uterine
leiomyomata. In that patient, embolization of a large uterine leiomyoma that
involved most of the uterus was performed, and potential etiologies for the
uterine necrosis included superinfection and poor collateral circulation
[5]. Pelage et al.
[9] also reported a case of
acute uterine necrosis with endometritis after uterine artery embolization in
a patient with a large submucosal uterine leiomyoma. Therefore, the large
diameter of a uterine leiomyoma was thought to be a predisposing factor for
uterine necrosis.
Cottier et al. [10]
reported the case of a patient with uterine necrosis occurring within months
after uterine artery embolization was performed for heavy postpartum
hemorrhage using smaller 150- to 250-µm PVA particles. The use of smaller
PVA particles may have led to this complication via occlusion of fine distal
arterial branches and prevention of collateral vessel formation, particularly
because the frequency of ischemia-related complications with such smaller PVA
particles during uterine artery embolization has been shown to be higher than
that observed with larger PVA particles
[9].
On MRI, the normal uterine myometrium shows intermediate signal intensity
on T1-weighted images (Fig.
4A), low to slightly high signal intensity on T2-weighted images
(with lower signal present in the inner myometrium than in the outer
myometrium) and diffuse enhancement on delayed gadolinium-enhanced T1-weighted
images [12,
13]. Immediately (within 30
min) after uterine artery embolization, myometrial perfusion becomes
considerably decreased (by a mean of approximately 75%) as measured on
dynamically enhanced MRI, whereas perfusion to uterine leiomyomata is
completely suppressed [13].
However, after 1–4 months, myometrial perfusion returns to normal,
whereas perfusion to uterine leiomyomata tends to remain suppressed
[13] (Figs.
4A and
4B). Myometrial perfusion is
preserved after uterine artery embolization because of a larger mean diameter
of myometrial vessels as compared with that of vessels to leiomyomata and a
generally greater microvascular density of the myometrium relative to that of
leiomyomata [13,
14]. In addition, collateral
flow through vessels, including the ovarian arteries, round ligament arteries,
cervical arteries, and other pelvic arteries, reconstitutes intrauterine
branches and maintains viability of the uterus
[3,
14]. However, small foci of
myometrial necrosis around uterine leiomyomata have occasionally been reported
after uterine artery embolization
[10].
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Fig. 4A. —49-year-old woman (separate patient) 1 month after uterine
artery embolization for symptomatic uterine leiomyomata without complication.
Axial fat-suppressed T1-weighted images (TR/TE/FA, 185/1.7/90) obtained before
(A) and after (B) contrast administration show absent
enhancement of treated leiomyomata (F) that are of high signal intensity
before contrast administration (A). Remainder of uterine myometrium (M)
shows normal enhancement.
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Fig. 4B. —49-year-old woman (separate patient) 1 month after uterine
artery embolization for symptomatic uterine leiomyomata without complication.
Axial fat-suppressed T1-weighted images (TR/TE/FA, 185/1.7/90) obtained before
(A) and after (B) contrast administration show absent
enhancement of treated leiomyomata (F) that are of high signal intensity
before contrast administration (A). Remainder of uterine myometrium (M)
shows normal enhancement.
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When the uterine myometrium has undergone necrosis, intermediate to high
signal intensity on T1-weighted images and high signal intensity on
T2-weighted images are depicted, along with a lack of early and delayed
enhancement. Similarly, necrosis of the endometrium may manifest as a lack of
endometrial enhancement on gadolinium-enhanced images. Residual spared areas
of viable myometrium may be present in the uterine periphery secondary to
superficial uterine pelvic collateral blood supply. Gas, if present, may
appear as very low signal intensity foci on both T1-weighted and T2-weighted
images, although none was visualized in our patient.
We hypothesize that uterine necrosis in our patient resulted from
insufficient collateral circulation to the uterus, although the underlying
reason for this is unknown. Currently, there are no data suggesting that prior
cesarean section, myomectomy, or oophorectomy increases the risk for uterine
necrosis following uterine artery embolization. Very large leiomyomata were
not present in our patient, and large PVA particles (> 300 µm) were used
during uterine artery embolization.
In summary, we present the clinical, pathologic, and MRI findings of a
patient with the rare complication of uterine necrosis after therapeutic
uterine artery embolization for symptomatic uterine leiomyomata, subsequently
requiring hysterectomy.
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Introduction
Case Report
