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Year : 2011  |  Volume : 54  |  Issue : 1  |  Page : 187-188
Arteriovenous malformation of uterus

Department of Histopathology, Royal Hospital, Muscat, Sultanate of Oman

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Date of Web Publication7-Mar-2011

How to cite this article:
Al-Shekaili KR, Bhatnagar G, Ramadhan FA, Al-Zadjali N. Arteriovenous malformation of uterus. Indian J Pathol Microbiol 2011;54:187-8

How to cite this URL:
Al-Shekaili KR, Bhatnagar G, Ramadhan FA, Al-Zadjali N. Arteriovenous malformation of uterus. Indian J Pathol Microbiol [serial online] 2011 [cited 2022 Jul 5];54:187-8. Available from: https://www.ijpmonline.org/text.asp?2011/54/1/187/77400

A 50-year-old lady presented with a history of irregular heavy period of 8 months duration. She was diagnosed to have gestational trophoblastic disease 12 years earlier. The patient is in remission for the last 11 years and is on routine follow-up. Her last beta - Human Chorionic Gonadotropin (B-HCG) was normal. There was also a history of complete abortion 4 years ago.

Physical examination revealed enlarged nontender uterus of 10 weeks size. Transvaginal scan showed enlarged uterus with highly vascular lesion in the endometrium invading the full thickness of the myometrium. Uterine carcinoma was suspected and the patient was referred to a tertiary hospital. On admission, the patient underwent magnetic resonance imaging (MRI), which showed large bulky anteverted uterus with increased thickness of myometrium compromising the endometrial canal. The anterior wall measured 3.8 cm. There were extensive areas of signal voids seen in the myometrium and serosal layer denoting extensive vascularity associated with extensively enlarged pelvic venous plexus. The right internal iliac vein was hugely distended [Figure 1]. No definite enhancing mass of the uterus was seen. In view of the extensive uterine and pelvic vascularity, absence of definite uterine mass and normal tumor markers, the imaging findings raised the possibility of large uterine arteriovenous malformation (AVM) rather than a uterine tumor.
Figure 1: MRI T2 image shows extensive areas of signal void in the myometrium and serosal layer

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The patient underwent total abdominal hysterectomy. We received a previously opened uterus, which measured 10.0 × 8.5 × 3.0 cm and weighed 153 g. The serosal surface was smooth. The cervical canal was patent and measured 2.9 cm, the endometrial cavity measured 5.6 cm, and endometrial thickness was 0.3 cm. The myometrium was 1.6 cm thick. The cut surface of bisected uterus showed dilated vessels with blood clots in the myometrium.

Microscopic examination of the uterus showed endometrium in the proliferative phase. The myometrium showed many ectatic congested thick-walled vessels. Vessels were of varying caliber and were seen up to the serosal aspect [Figure 2].
Figure 2: Ectatic thick vessels in the myometrium (H and E, ×200)

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The overall features were consistent with the uterine AVM.

AVM is an abnormal connection between veins and arteries. It can occur in various parts of the body, such as the brain, spleen, lung, kidney, liver, intercostal spaces, iris, and spermatic cord. In 1926, Dubreuil and Loubat reported the first case of AVM as cited by Bagga et al.[1] AVM of the uterus is a rare condition with less than 100 cases reported in the literature. [1] Although AVM is most commonly congenital, genetic transmission patterns are unknown.

Acquired uterine AVMs are preceded by a surgery, such as curettage, caesarean section or hysterectomy, pelvic trauma, previous pregnancy, gestational trophoblastic disease, exposure to diethylstilbesterol, endometriosis, fibromyoma, and endometrial or cervical cancers. The clinical scenario varies from silent, nonharmful condition to potentially life-threatening condition. The patients with uterine AVM may present with sudden profuse vaginal bleeding. Most commonly the bleeding is intermittent and torrential. [2]

In the present case, the AVM is of the acquired type. Two factors appear to be contributing to the condition: gestational trophoblastic disease and abortion.

An accurate diagnosis is important for prompt management, as this condition could be fatal if undiagnosed early. Angiography is the gold standard of diagnosis of uterine AVM. However, Doppler ultrasound is used frequently as a good, noninvasive modality of diagnosis. [3] Endovaginal sonography with gray scale, color, and spectral Doppler imaging of the AVM cases is nonspecific and shows subtle myometrium heterogeneity. In addition, color Doppler sonography reveals a tangle of vessels with multidirectional high-velocity flow that produce a "color mosaic" pattern, whereas arteriovenous shunting with high-velocity, low-resistance flow was seen by spectral Doppler analysis. [3]

In this case, the patient underwent transvaginal ultrasound initially, which showed vascular lesion in the uterus; however, the diagnosis of uterine AVM was made by MRI.

MRI is helpful in determining the size and extent of the lesion. The characteristic feature of uterine AVM in MRI is multiple signal voids corresponding to the tangle of vessels demonstrated by Doppler ultrasound. Management of uterine AVM varies from conservative medical management to more definite surgical management. The choice of management modality depends on many factors: patient age, the desire of future fertility, severity of the bleeding, and the size and site of the lesion.

Uterine AVM has been successfully treated by uterine artery embolization. However, some authors postulate that large lesions involving the subendometrial tissue usually require surgical intervention.

Uterine artery embolization reduces hospital stay, ensures faster recovery, and does not interfere with future fertility. [4] Moreover, successful cases of postembolization pregnancy were reported. AVM was managed successfully by ligation of the feeding artery. [5] Our patient underwent hysterectomy.

In conclusion, uterine AVM is a rare condition, but potentially life-threatening. Recently, however, new radiologic modalities show that this condition is not as rare as previously thought.

   References Top

1.Bagga R, Verma P, Aggarwal N, Suri V, Bapuraj JR, Kalra N. Failed Angiographic Embolization in Uterine Arteriovenous Malformation. Medscape J Med 2008;10:12.  Back to cited text no. 1
2.O'Berien P, Neyastani A, Buckley AR, Chang SD, Legiehn GM. Uterine arteriovenous malformation from diagnosis to treatment. J Ultrasound Med 2006;25:1387-92.  Back to cited text no. 2
3.Wiebe ER, Switzer P. Arteriovenous malformation of uterus associated with medical abortion. Int J Gynecol Obstet 2000;71:155-8.  Back to cited text no. 3
4.Patel S, Potti S, Jaspan D, Dandolu V. Embolization of uterine arteriovenous malformation for treatment of menorrhagia. Arch Gynecol Obstet 2009;279:229-32.  Back to cited text no. 4
5.Yokomine D, Yoshinaga M, Baba Y, Mastuo T, Iguro Y. Successful arteriovenous malformation by ligation of feeding artery after unsuccessful uterine artery embolization. J Obstet Gynaecol Res 2008;35:183-8.  Back to cited text no. 5

Correspondence Address:
Khaloud R Al-Shekaili
Department of Histopathology, Royal Hospital, Muscat, Sultanate of Oman

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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.77400

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