Case report of recurrent uterine arteriovenous malformation
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A 35-year-old female presented to us with secondary post-partum hemorrhage after 12 days delivery of macerated stillbirth (MSB) at term via induction of labor. The delivery was uneventful and she was discharged two days later. She has a previous history of cesarean section four years ago due to placenta previa, which complicated with massive post-partum hemorrhage, required blood transfusions. Upon examination, she was hemodynamically stable and afebrile. However, she looked pale with a hemoglobin level of 6.7 g/dL. The uterus was palpable at 20-week size with the normal cervix and parous os. She was transfused with 4 pints packed cells. The transabdominal scan showed an endometrial thickness of 11.2 cm, irregular margin, and mixed echogenicity. The provisional diagnosis was endometritis and broad-spectrum antibiotics were commenced but the symptoms did not improve. Repeat ultrasound with Doppler showed solitary intrauterine mass 15.7 mm x 33.4 mm with areas of high vascularity within the myometrium, differential diagnosis of the retained product of conception, placenta accreta or placenta site trophoblastic tumor (PSTT) were made but serial serum beta-human chorionic gonadotropin (hCG) level showed decreasing in trend from 125.7–20.1 mIU/mL.

Surgical evacuation of uterine cavity removed blood clots only with no product of conception. MRI scan of pelvis showed a bulky uterus, widened with heterogeneous, highly vascular lesion extending into the myometrium with clear demarcation with the surrounding area. Features are suggestive of hypervascular lesion of the anterior uterus. The impression of uterine arteriovenous malformation or PSTT was made. She was referred to an interventional radiologist for pelvic angiogram and embolization of the lesion for the intractable genital tract bleeding. The uterine artery angiogram revealed arteriovenous malformation in both hemipelvis. The first embolization procedure with polyvinyl alcohol (PVA) 355–500 microns was performed to block the bilateral uterine arteries. The genital tract bleeding was reduced remarkedly. One year later, this patient presented to us with a new episode of profuse genital tract bleeding, pelvic MRI scan was done to confirm the arteriovenous malformation recurrence, and it did show evidence of residual arteriovenous malformation. Angiography demonstrated new fine feeders from the right uterine artery, which was successfully embolized using polyvinyl alcohol.

This lady remained asymptomatic until three years later with the latest pelvic ultrasound showed bilateral abnormal and prominent vessels on right and left myometrium with prominent draining veins more on the right side. She was explained that her uterine arteriovenous malformation was likely acquired from her previous cesarean or regrowth of the arteriovenous malformations as a result of the persistence of unknown inherent factors. They may regress spontaneously or rupture, which may cause genital tract bleeding and complicating future pregnancy. Treatment options were discussed and she chose to undergo third uterine artery embolization. The uterine artery angiogram confirmed the presence of an arteriovenous malformation in the right lateral wall region, originating from a right uterine artery, which was successfully treated by embolization. The patient was discharged well after the successful procedure. She is still under our gynecological outpatient follow-up.