CASE 18550 Published on 10.05.2024
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Embolisation of uterine arteriovenous malformation: Dispersing a looming threat

Section

Interventional radiology

Case Type

Clinical Case

Authors

Deepthi Sethumadhavan 1, Sabareesh Suresh Kumar 2, Prabakaran M. S. 1

1 Department of Radiology, KG Hospital, Coimbatore, Tamil Nadu, India

2 Department of Interventional Radiology, KG Hospital, Coimbatore, Tamil Nadu, India

Connected authors
Patient

26 years, female

Categories
Area of Interest Genital / Reproductive system female, Interventional vascular, Vascular ; Imaging Technique Catheter arteriography, MR, Ultrasound-Colour Doppler
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Clinical History

A 26-year-old female with a history of one miscarriage, which was treated by dilatation and curettage 45 days back, reported an episode of severe vaginal bleeding.

Imaging Findings

Pelvic MRI (Figures 1a, 1b, 1c and 1d) show uterine intracavitary heterogeneous soft tissue mass with multiple flow voids causing obliteration of the lower anterior junctional zone and mild myometrial thinning.

Transabdominal colour Doppler US (Figure 2) demonstrated significant myometrial hypervascularisation with low-resistance and high-velocity flow.

An arteriogram of the uterine artery showed a nidus of blood vessels arising from the uterine artery with early venous filling (Figures 3a, 3b, 3c, 4a, 4b and 4c).

Discussion

Background

Uterine arteriovenous malformation (AVM) is a rare vascular anomaly in which there is enlargement of the intervillous space deep inside the myometrium, thereby causing direct flow from the arterial system towards the venous system without the capillary bed [1]. It is usually caused by reactive angiogenesis triggered due to pregnancy-related changes, uterine procedures, or trophoblastic invasion [3]. Uterine instrumentations, especially dilatation and curettage, are primary contributors to uterine AVMs since they induce inflammation and reactive formation of new vessels [3].

Clinical Perspective

Typically, these lesions manifest in women of reproductive age. The predominant symptoms are excessive menstrual bleeding (menorrhagia) and irregular uterine bleeding (menometrorrhagia). Additional symptoms include recurrent spontaneous abortions, lower abdominal discomfort, painful intercourse (dyspareunia), and anaemia.

Imaging Perspective

USG reveals an ill-defined heteroechoic mass with multiple anechoic vascular cystic spaces in the endometrial cavity. Doppler US shows low-resistance and high-velocity flow [2]. MRI with contrast reveals the disease extent and helps in confirming the diagnosis. It shows an enlarged uterus with an ill-defined hyper enhancing mass having multiple serpentine flow voids. There is focal or diffuse interruption of the junctional zone. On contrast, these vessels enhance with early venous drainage [2]. Digital subtraction angiography is the gold standard for diagnosing uterine AVMs. It is usually taken in cases that need definite treatment by endovascular embolisation. It shows the arterial supply to the AVM, whether it is unilateral or bilateral, the size of the nidus, and also early venous drainage, thereby differentiating it from enhanced myometrial vascularity [4].

Outcome

Transcatheter embolisation is the treatment of choice for these acquired vascular abnormalities since fertility can be preserved by this procedure. It targets only the arterial feeders involved, thereby maintaining vascularity in the rest of the uterus [4].

For our patient, under all aseptic precautions and local anaesthesia, the right common femoral artery was punctured, and a 5-French sheath was secured. Using a 5-French RAC catheter, bilateral internal iliac arteries were selectively cannulated, and an angiogram was performed. The arterial feeders were superselectively cannulated using a microcatheter and microwire (0.014 inch), and embolisation was done using Polyvinyl Alcohol Foam (PVA) particles (500–710 microns). The control angiogram revealed complete obliteration of the parenchymal blush (Figures 3c and 4c). The follow-up MRI showed complete resolution of the lesion with a normal uterus (Figures 5a and 5b).

Teaching Points

Uterine AVMs should be considered in patients presenting with menorrhagia with a recent history of uterine instrumentations, such as dilatation and curettage, or other risk factors [2].

Written informed patient consent for publication has been obtained.

Differential Diagnosis List
Retained products of conception (RPOC)
Uterine arteriovenous malformation (AVM)
Gestational trophoblastic disease (GTD)
Final Diagnosis
Uterine arteriovenous malformation (AVM)
Case information
URL: https://www.eurorad.org/case/18550
DOI: 10.35100/eurorad/case.18550
ISSN: 1563-4086
License

This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.

Figure 1

Pelvic MRI

Axial T2-weighted TSE sequence shows uterine intracavitary heterogeneous soft tissue mass measuring with multiple vascular-like serpiginous structures characterised by flow void causing obliteration of lower anterior junctional zone and mild myometrial thinning.
Axial T2-weighted TSE sequence shows uterine intracavitary heterogeneous soft tissue mass measuring with multiple vascular-like serpiginous structures characterised by flow void causing obliteration of lower anterior junctional zone and mild myometrial thinning.
Coronal T2-weighted TSE sequence shows uterine intracavitary heterogeneous soft tissue mass measuring with multiple vascular-like serpiginous structures characterised by flow void causing obliteration of lower anterior junctional zone and mild myometrial thinning.
Coronal T2-weighted TSE sequence shows uterine intracavitary heterogeneous soft tissue mass measuring with multiple vascular-like serpiginous structures characterised by flow void causing obliteration of lower anterior junctional zone and mild myometrial thinning.
Sagittal T2-weighted TSE sequence shows uterine intracavitary heterogeneous soft tissue mass measuring with multiple vascular-like serpiginous structures characterised by flow void causing obliteration of lower anterior junctional zone and mild myometrial thinning.
Sagittal T2-weighted TSE sequence shows uterine intracavitary heterogeneous soft tissue mass measuring with multiple vascular-like serpiginous structures characterised by flow void causing obliteration of lower anterior junctional zone and mild myometrial thinning.
The mass shows brisk early contrast enhancement with a tuft of vessels within seen contiguous with prominent parametrial vessels.
The mass shows brisk early contrast enhancement with a tuft of vessels within seen contiguous with prominent parametrial vessels.
Figure 2

Transabdominal colour Doppler US

Transabdominal colour Doppler US demonstrating intense myometrial hypervascularisation with turbulent flow.
Transabdominal colour Doppler US demonstrating intense myometrial hypervascularisation with turbulent flow.
Figure 3

Arteriogram of the right uterine artery

Arteriogram of the right uterine artery demonstrating a nidus of blood vessels (black arrow) arising from the right uterine artery (white arrow).
Arteriogram of the right uterine artery demonstrating a nidus of blood vessels (black arrow) arising from the right uterine artery (white arrow).
Arteriogram of the right uterine artery demonstrates the vascular nidus of the uterine AVM (black arrow) with early opacification of the right internal iliac vein (white arrow).
Arteriogram of the right uterine artery demonstrates the vascular nidus of the uterine AVM (black arrow) with early opacification of the right internal iliac vein (white arrow).
Arteriogram post-embolisation showing the absence of filling of the occluded right uterine artery and vascular malformation.
Arteriogram post-embolisation showing the absence of filling of the occluded right uterine artery and vascular malformation.
Figure 4

Arteriogram of the left uterine artery

Arteriogram of the left uterine artery demonstrating a nidus of blood vessels (white arrow) arising from the left uterine artery (black arrow).
Arteriogram of the left uterine artery demonstrating a nidus of blood vessels (white arrow) arising from the left uterine artery (black arrow).
Arteriogram of the left uterine artery demonstrates the vascular nidus of the uterine AVM (white arrow) with early opacification of the left internal iliac vein (black arrow).
Arteriogram of the left uterine artery demonstrates the vascular nidus of the uterine AVM (white arrow) with early opacification of the left internal iliac vein (black arrow).
Arteriogram post-embolisation showing the absence of filling of the occluded left uterine artery and vascular malformation.
Arteriogram post-embolisation showing the absence of filling of the occluded left uterine artery and vascular malformation.
Figure 5

Follow-up Pelvic MRI

After 3 months, the sagittal T2-weighted TSE sequence shows total resolution of the intracavitary component of previously documented arteriovenous malformation.
After 3 months, the sagittal T2-weighted TSE sequence shows total resolution of the intracavitary component of previously documented arteriovenous malformation.
After 3 months, the coronal T2-weighted TSE sequence shows total resolution of the intracavitary component of previously documented arteriovenous malformation.
After 3 months, the coronal T2-weighted TSE sequence shows total resolution of the intracavitary component of previously documented arteriovenous malformation.