Successful treatment of uterine arteriovenous malformation

Uterine arteriovenous malformation (AVM) is defined as abnormal and nonfunctional connections between the uterine arteries and veins. Although rare, it is a potentially life-threatening condition. Fewer than 100 cases are reported in existing literature and include patients who presented with per vaginam (PV) bleeding, often mild to moderate, but sometimes life-threatening. It is likely to occur during a woman’s reproductive years and treatment depends on signs and symptoms, as well as future fertility requirements. If symptoms are not improved with conservative treatment, uterine artery embolisation is required to avoid the need for a hysterectomy.

This report looks at a case of acquired uterine AVM, confirmed by angiography, which was successfully treated with bilateral uterine artery embolisation.

Introduction

There are two types of AVM in the uterus: one is congenital and the other is acquired through previous uterine trauma (eg. curettage or previous pelvic operations), infection or trophoblastic disease. Congenital AVM is extremely rare, whereas acquired AVM is increasing in incidence. This rare condition occurs most frequently in women of reproductive age. Such women present most commonly with PV bleeding but some present with life-threatening bleeding. Management of AVM is mostly conservative but may necessitate embolisation.

Case report

A 30-year-old female (P3+1) presented at the emergency department at 6+ weeks gestation with mild pain and PV bleeding; following a scan, she was discharged home. She subsequently presented at the early pregnancy assessment unit (EPAU) for a further scan to confirm dates and the viability of her pregnancy. She was diagnosed with a missed miscarriage at 7+3 weeks and a plan was made for medical management. She received mifepristone and full doses of misoprostol, neither of which had any effect for two days. She was then booked for an evacuation of retained products of conception (ERPC). Her haemoglobin (Hb) levels were 12g/dl. During the ERPC, she bled > 2 litres within 25 minutes and required four units of blood transfusion.

The patient was managed via ERPC under ultrasound (US) guidance and then via a Foley catheter in her uterine cavity, filled with 30ml. The bleeding stopped and the catheter was removed after 24 hours. There was minimal bleeding and the patient was discharged home on day two with Hb 9.6g/dl and on oral iron.

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She then had continuous mild vaginal bleeding and some episodes of heavy bleeding. She had multiple admissions and underwent a departmental ultrasound where a hypodense mass of approximately 6 x 7cm was found in the lower part of her uterus, with an increased blood supply in periphery of mass. An MRI scan revealed a hypodense mass of approximately 6 x 7cm with prominent peri-uterine and pelvic plexus of veins, as well as a left gonadal vein with prominent suspicion of AVM of the uterine arteries. The patient then underwent a pelvic angiogram, which was suggestive of AVM, before being referred for bilateral uterine artery embolisation, with polyvinyl alcohol to preserve her fertility. After embolisation, the patient’s condition was greatly improved. She had experienced continuous mild bleeding for a month and a half with the occasional episode of heavy bleeding but following the embolisation, she experienced no further bleeding. Improvement was evident 10 days after the embolisation. She also underwent a pelvic ultrasound after three weeks of embolisation, the results of which were normal.

Discussion

As mentioned, uterine AVM is a rare condition. Congenital AVM is extremely rare and, while also rare, the incidence of acquired AVM is on the rise. Congenital AVM arises from arrested vascular embryologic development and results in abnormal differentiation in capillaries and abnormal communication between arteries and veins. It can have multiple vascular connections and may invade surrounding structures. The most important factor to consider with this condition is accurate and timely diagnosis, as well as appropriate treatment, as AVM may cause life-threatening heavy vaginal bleeding or continuous PV bleeding.

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The diagnosis of AVM is made easier with colour Doppler ultrasound. The differential diagnoses of AVM are retained products of conception (RPC) and gestational trophoblastic disease (GTD). These conditions also increase vascularity and turbulence flow.

Previously, AVM was diagnosed on laparotomy or during hysterectomy. Nowadays, however, high resolution colour Doppler US can accurately diagnose AVM. The difficulty with this method of diagnosis lies in the differentiation between arterial and venous waveforms, as the blood flow in AVM is multidirectional and forms an abnormal pattern. With AVM, beta human chorionic gonadotropin (BHCG) does not rise but patients produce high levels of human placental lactogen.

In our case, BHCG was measured and was normal. Our patient also had a previous history of missed miscarriage and ERPC, either of which may have caused the acquired AVM.

This case is a strong example of acquired AVM successfully treated with bilateral uterine artery embolisation.

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