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” should be changed to “enhanced myometrial vascularity.”¹⁶ For this reason our recently published article on the subject already uses the new terminology.¹⁷

The Diagnosis of EMV

Historically, the diagnosis of an EMV was made following laparotomy. Subsequently, angiography became the gold standard technique and is still used at the time of the UAE process.¹⁸ Recently, transvaginal sonography (TVS) “grayscale” and color or power Doppler ultrasound (US) became the primary diagnostic tool used to triage and follow patients with EMV, leaving angiography as a therapeutic tool. Despite the advantage and ease of US diagnosis of EMV, in a review of the subject Toulhami et al¹⁹ still considers CT angiography as the “gold standard” to diagnose the pathology.

Grayscale (black and white) US characteristics are nonspecific and include the presence of irregular hypoechogenic, tortuous, and tubular structures within the myometrium. Without using Doppler interrogation they are easily missed, except if they show a large area of unusually large “lakes” with active blood flow. A “panoramic” grayscale image of the sagittal US image of the uterus in question should be followed by color (or power) Doppler interrogation focusing on suspicious areas for more information (Figure 9-1). The severity of the EMV is expressed by the velocity of the blood flow measured as “peak systolic velocity” (PSV) while the resistance of the vessel wall to flow is expressed as “resistance index” (RI). The higher the PSV, the lower the RI and the more severe the pathology is. The simplest method to detect the blood vessel with the highest velocity blood flow is to scroll through consecutive sagittal sections of the uterus and sample the vessel that demonstrates the most “concentrated” f color signals. Our group uses another, probably more accurate, method that is based upon gradually increasing the PRF until only a few vessels are seen²⁵ (Figure 9-2). The lower the PRF, the more vessels will show. The higher the PRF, the less sensitive it is to pick-up flow; therefore, only vessels with the highest velocity flow will be visible. We measure the PSV only if such a blood vessel is apparent. The PSV obtained using this method is the one we use in clinical management.