SI Mohamed1, MBBS, MRad, BJJ
Abdullah1, MBBS, FRCR, SZ Omar2,
1 Department of Biomedical Imaging (Radiology), Faculty of
Medicine, University of Malaya, Kuala Lumpur, Malaysia
2 Department of Obstetric and Gynaecology, Faculty of Medicine,
University of Malaya, Kuala Lumpur, Malaysia
A 30-year-old Malay female presented with massive secondary
postpartum haemorrhage three weeks after a complicated vaginal
delivery. There was difficulty in the delivery of the placenta
at delivery and it was only delivered completely after 30
minutes by controlled cord traction. She was also treated
with 40 units oxytocin infusion to prevent postpartum haemorrhage.
Blood loss was minimal and estimated at 250 ml. She also had
a previous history of a pregnancy being complicated by retained
placenta where manual removal of the placenta under general
anaesthesia was required. Her menarche was at 14 years and
before that pregnancy she had a normal menstrual pattern.
Physical examination revealed a mildly pale young woman
with blood pressure of 100/60 mmHg and pulse rate of 90 beats
per minute. Gynaecological examination revealed a slightly
enlarged, retroverted, mobile and non-pulsatile uterus. There
were large blood clots in the vagina and nominal active vaginal
bleeding from a normal-appearing cervical os. No cervical
or vaginal lacerations were observed. Laboratory evaluation
revealed mild anaemia with haemoglobin count of 10.0 g/L and
a normal platelet count of 178,000. Coagulation profile and
serum beta-HCG level were within normal limits.
In view of bulky uterus, transvaginal ultrasonography pelvis
was performed to rule out intrauterine pathology (Figure 1).
[View this figure]
|Figure 1 Transvaginal colour Doppler ultrasound (printed in grey scale) of the uterus in the sagittal plane.
- What does the ultrasound image show?
- What is the underlying pathological process?
- What are the known causes of this abnormality?
- What are the other clinical presentations?
- What other imaging modalities can be used
- What treatment options are available?
Arteriovenous malformation of the
uterus: a rare cause of secondary postpartum haemorrhage
Ultrasonography reveals mixed echogenicities within the uterine
cavity with multiple anechoic spaces within the myometrium
at the uterine fundus and body. These cystic spaces demonstrated
colour signals and high velocity flow with a low resistive
index at colour Doppler ultrasonography consistent with a
diagnosis of uterine arteriovenous malformation (AVM) (Figure
[View this figure]
|Figure 1 Transvaginal colour Doppler ultrasound (printed in grey scale) of the uterus in the sagittal plane demonstrates colour signals with high velocity blood flow within the myometrium at the uterine fundus (yellow arrow) and body (red arrow).
AVMs of the uterus are rare and were first described by Dubreuil
and Loubat in 1926 . An AVM consists
of a proliferation of arterial and venous channels with fistula
formation and an admixture of small, capillary-like channels.
The size of these vessels varies considerably, which probably
accounts for the variety of descriptive terms found in the
literature [1,2]. The
true incidence of uterine AVMs is unknown since to date only
case reports or small case series exist, making it impossible
to provide a true incidence . It is known
that AVMs are more common in women and have a predilection
for the pelvic blood vessels. Since then, several terms have
been used to refer to these lesions, including cavernous haemangioma,
cirsoid aneurysm, racemose aneurysm, arteriovenous aneurysm,
pulsatile angioma, and arteriovenous fistula.
Uterine AVMs may be congenital or acquired. In the congenital
variety, there is failure of differentiation into artery and
vein with the ultimate presence of multiple anastomoses between
the two as well as involving the surrounding muscles, skin
or viscera . Even though it is generally
accepted that acquired malformation may be due to previous
uterine trauma (prior pelvic operation, curettages), intrauterine
contraceptive devices, pathologic pregnancy-related events,
and the treatment of endometrial carcinoma and gestational
trophoblastic disease  resulting in a
abnormal communication between adjacent artery and vein, it
has been suggested that these procedures may only cause a
clinically silent congenital malformation to manifest. In
addition, the effect of hormones on AVMs further confuses
the issue. Nevertheless in view of the patient’s history
of previous pregnancy complicated by retained placenta, this
may indicate an acquired aetiology. In addition, the absence
of symptoms prior to this, the presence of a single communication
between artery and vein, plus the absence of investment of
surrounding tissues makes an acquired aetiology highly likely.
Doppler and magnetic resonance (MR) imaging features of uterine
AVMs may overlap with other causes of arteriovenous shunting,
including abnormal placentation and gestational trophoblastic
disease (GTD). These can be differentiated with serum beta
human chorionic gonadotropin (HCG) tests results (negative
with AVM, positive with GTD) .
Even though the clinical presentation of uterine AVMs is highly
variable, the most common presenting complaint is excessive
vaginal haemorrhage or menorrhagia, which requires blood transfusions
in 30% of reported cases [6,7].
Other uncommon presentations include postpartum haemorrhage
like in this patient, postmenopausal bleeding and congestive
heart failure secondary to a vascular steal syndrome [2,3].
Additionally, a number of cases of asymptomatic uterine AVMs
have been found incidentally at the time of hysterectomy .
Age and prior pregnancy have little value in making a diagnosis.
The presence of a palpable arterial pulsation on bimanual
examination or the presence of a pulsating mass on hysteroscopy
should increase the clinician’s suspicion for AVMs.
Uterine AVMs can be diagnosed by using ultrasonography, contrast-enhanced
computed tomography, MR imaging and angiography .
The greyscale ultrasonography (US) may demonstrate prominent
parametrial vessels, a normal appearing endometrium and multiple
distinct anechoic spaces in the myometrium without mass effect.
On colour Doppler US, these cystic spaces generate colour
signals in a mosaic pattern representing turbulent flow. These
appearances were seen in this patient. Spectral analysis of
the arterial vessels within the lesion shows high-velocity
flow with a low resistive index (approximately 0.51-0.65).
Spectral analysis of venous flow demonstrates a similar pattern
[2,6]. However, the ability
of Doppler US to depict the precise extent of the lesion within
the pelvis may be limited even with transvesical or endovaginal
ultrasound. Doppler US however is the initial method of choice
and the preferred method for following up patients after treatment
MR imaging may be performed to confirm a diagnosis and delineate
the extent of AVM . MR imaging may show
a bulky uterus, a focal uterine mass, disruption of the junctional
zones, serpiginous flow-related signal voids, and prominent
parametrial vessels . The definitive diagnosis has been
traditionally made using angiography and it is well documented
in the literature [1,3-5,7].
Pelvic angiography in this patient revealed serpiginous, dilated
and tortuous vessels in the uterus, supplied primarily by
the right uterine artery with a small contribution from the
left uterine artery (Figure 2). Early large draining veins
and nidus of the AVM were noted at the end of the arterial
phase (Figure 3).
[View this figure]
|Figure 2 Selective catheterization
of right uterine artery (blue arrow) demonstrates
dilated, tortuous and serpiginous vessels supplying
the fundus (yellow arrow) and body of the uterus
[View this figure]
|Figure 3 Large early draining
veins (yellow arrow) and nidus (red arrow) of the
uterine arteriovenous malformation are noted at
the end of the arterial phase.
The treatment of uterine AVM depends on the severity of vaginal
bleeding, the patient’s age and her future fertility
desires. If the patient is asymptomatic, no treatment is required
. Acute treatment consists of haemodynamic
stabilization and management of active bleeding. Ultimate
treatment depends on the patient’s reproductive desires
[2,3]. In the past treatment
has been confined to hysterectomy, but this carries significant
morbidity and in women of reproductive years is associated
with considerable psychological distress. Recent reports have
described successful treatment by embolisation, with subsequent
pregnancies indicating preservation of uterine function [3,8]
though this is still controversial. Embolisation performed
simultaneously with angiography can provide both diagnosis
and treatment during the same procedure.
In the case presented, hysterectomy was discussed as definitive
therapy but the patient expressed a desire to retain the uterus
if at all possible to attempt future pregnancy. The patient
was transfused with three units of whole blood and after haemodynamic
stabilisation; percutaneous transfemoral pelvic angiography
was performed with a view for embolisation. Both uterine arteries
were selectively embolised using a 5F Roberts Uterine Curve
catheter (Cook Incorporated, Bloomington, USA) with one vial
300-500 µm polyvinyl alcohol particles (Cook Incorporated,
Bloomington, USA) (Figure 4). After the procedure, no arterial
flow could be demonstrated, and the post procedure course
in ward was uneventful. During a follow-up period of six months
after the embolisation, the patient has had normal menses
without excessive bleeding and no pelvic complaints.
[View this figure]
|Figure 4 The large uterine arteriovenous
malformation is successfully embolised using polyvinyl
alcohol particles (PVA).
Embolic agents, which can be used for uterine vessels, include
polyvinyl alcohol (PVA) particles, absorbable gelatine sponge
(Gelfoam; Pharmacia and Upjohn, Kalamazoo, MI), metallic coils,
and glue (N-butyl cyanoacrylate, Histoacryl; B. Braun, Melsungen,
Germany). The basis of embolic agent selection depends largely
on operator preference and expertise; in those with expertise
with the use of glue as an embolic agent for neural AVMs prefers
it to other agents. Conversely, PVA particles and absorbable
gelatine sponge are preferred by the others and is indicated
in cases in those patients where selective embolisation of
nidus feeding vessels is not technically possible. Micro-catheters
are used when standard angiographic catheters cannot be advanced
into the distal uterine artery or branches of the uterine
artery as a result of vessel size, tortuosity, and/or spasm.
Uterine AVM should be included in the differential diagnosis
in patients with excessive postpartum haemorrhage. Colour
and spectral flow Doppler US can aid diagnosis and clinical
management. Conservative treatment by uterine artery embolisation
should also be considered in the treatment of these lesions
as it appears safe and effective .
Fleming H, Ostor AG, Pickel H, et al. Arteriovenous malformations of the uterus. Obstet Gynecol 1989;73(2):209-14.
Polat P, Suma S, Kantarcy M, et al. Color Doppler US in the evaluation of uterine vascular abnormalities. Radiographics 2002;22(1):47-53.
Hoffman MK, Meilstrup JW, Shackelford DP, et al. Arteriovenous malformations of the uterus: an uncommon cause of vaginal bleeding. Obstet Gynecol Surv 1997;52(12):736-40.
Ghosh TK. Arteriovenous malformation of the uterus and pelvis. Obstet Gynecol 1986;68(3 Suppl):40S-3S.
Markoff G, Quagliarello J, Rosen RJ, et al. Uterine arteriovenous malformation successfully embolized with a liquid polymer, isobutyl 2-cyanoacrylate. Am J Obstet Gynecol 1986;155(3):659-60.
Huang MW, Muradali D, Thurston WA, et al. Uterine arteriovenous malformations: gray-scale and Doppler US features with MR imaging correlation. Radiology 1998;206(1):115-23.
Demir B, Dilbaz S, Haberal A, et al. Acquired uterine arteriovenous malformation after Caesarean section. Aust N Z J Obstet Gynaecol 2004;44(2):160-1.
Nicholson AA, Turnbull LW, Coady AM, et al. Diagnosis and management of uterine arterio-venous malformations. Clin Radiol 1999;54(4):265-9.
|Received 8 August 2005; received
in revised form 28 September 2005; accepted 7 October
Correspondence: Department of Biomedical Imaging (Radiology), University of Malaya Medical Centre, 59100 Kuala Lumpur, Malaysia.. Tel.: 603-79502069; Fax: 603-79581973; E-mail: firstname.lastname@example.org (Basri Johan Jeet Abdullah).
Please cite as: SI Mohamed, BJJ Abdullah,
Postpartum haemorrhage, Biomed Imaging Interv J 2005; 1(2):e13