Arteriovenous malformation (AVM): a faulty connection, or “short circuit,” between the arterious and venous supply of an organ.
Enhanced myometrial vascularity (EMV): increased blood flow in the myometrium following and/or associated with an abnormal pregnancy.
Peak systolic velocity (PSV): the maximum blood flow velocity within a blood vessel, obtained with color Doppler.
Uterine artery embolization (UAE): minimally invasive procedure used to reduce the blood flow in the uterine arteries.
Clinically, enhanced myometrial vascularity (EMV), formally known as uterine arteriovenous malformation (AVM), is a relatively uncommon iatrogenic vascular lesion that may cause life-threatening hemorrhage.1 EMV may occur when the thin wall of the abnormal vessels are disrupted after menstruation, miscarriage, or after uterine instrumentation. An EMV/AVM is a pathological phenomenon described as a faulty “short circuit” of the blood stream between an organ’s arterial and venous supply. The blood stream assumes an unusually high velocity, rendering the vessels into a vascular fistula. EMVs have been reported in patients between ages 18 and 72 years and are classified as congenital or acquired.2 The acquired ones usually result from pevious uterine surgery such as diagnostic or therapeutic dilation and curettage (D&C), cesarean section (CS), or myomectomy.3-5 Wiebe and Switzer6 reported 7 cases of uterine EMVs associated with and occurring after medical termination of pregnancy. They were initially suspected by the history of prolonged bleeding after medical abortion and then confirmed by color Doppler scanning. All cases were managed expectantly and resolved spontaneously.
Uterine EMVs are seen almost exclusively in women in their reproductive years with no history of pregnancy. All EMVs involve abnormal communication between the branches of the UA and the venous plexuses within the myometrium. Recently, a connection between cesarean scar pregnancy (CSP) and acquired EMV was recognized.7-12
As far as its histopathological aspect is concerned, an EMV can be caused by the erosive property of the syncitiotrophoblastic tissue and chorionic villi during normal or abnormal placentogenesis, including CSP.8 Others regard EMVs as errors in morphogenesis without any spontaneous regression composed of tortuous vascular channels that are lined by endothelium surrounded by abnormal mural cells. They called them “vascular lesions” unless diagnosed as EMVs by angiography or by pathology. They also theorize that after termination of pregnancy the villi show vascularity and fibrosis, leading to retained POCs at Doppler testing.13 Timmerman et al suggest that EMVs represent a subinvolution of the placental bed with failed obliteration of its vessels in the absence of RPOCs after cessation of the pregnancy. This explains the severe bleeding following the case of a delayed postabortal hemorrhage, or for that matter, after D&C of a CSP.14,15
Following a scientific session and discussion at the annual meeting of the International Society of Ultrasound in Obstetrics and Gynecology in Montreal (Oct 2015) it was proposed that the term “arteriovenous malformation” ...