Enhanced myometrial vascularity

Last revised by Daniel J Bell on 26 Aug 2022

Enhanced myometrial vascularity (EMV), often misdiagnosed as an acquired uterine arteriovenous malformation, is the presence of transiently increased blood flow within the uterine myometrium, typically associated with complications of pregnancy. 

Somewhat confusingly, the term “enhanced myometrial vascularity” has been used interchangeably with “uterine arteriovenous malformation” in the literature to describe the sonographic appearance of a hypervascular lesion within the uterine myometrium that demonstrates turbulent flow. However, there is a growing understanding that the vast majority of these lesions do not actually represent true arteriovenous malformations 1,2. Thus at the 2015 annual World Congress of the International Society of Ultrasound in Obstetrics and Gynecology (ISUOG), it was recommended that “enhanced myometrial vascularity” is the preferred term for what was previously known as an “acquired uterine arteriovenous malformation” 3

Enhanced myometrial vascularity is almost exclusively seen in the context of recent pregnancy, and therefore occurs in women of reproductive age 4. It is typically secondary to retained products of conception in the early postpartum period, or following first-trimester miscarriage or termination of pregnancy 1,5,6. However, the incidence of enhanced myometrial vascularity following a first-trimester miscarriage is relatively low (1.5%) 1. There is also a high association with cesarean scar pregnancy and gestational trophoblastic disease 4

Other less common causes of increased myometrial blood flow include 5,7:

Enhanced myometrial vascularity is readily visualized on transvaginal color Doppler ultrasound, as well as on CT or MR angiography. However, true uterine arteriovenous malformations appear identical on these modalities, and can only be distinguished from enhanced myometrial vascularity on digital subtraction angiography, which is considered the gold standard 1. The diagnosis of enhanced myometrial vascularity is therefore heavily reliant on the clinical context, particularly a history of recent pregnancy. Given that true uterine arteriovenous malformations (both congenital and acquired) are exceedingly rare 1,4, the vast majority of “uterine arteriovenous malformations” encountered in clinical practice are in fact enhanced myometrial vascularity.

Patients range from being asymptomatic to having profuse vaginal bleeding and subsequent anemia. A history of recent pregnancy is typical.

Enhanced myometrial vascularity is not considered a true arteriovenous malformation, which is defined as an abnormal anastomosis between an artery and vein that bypasses the capillary bed, a process that occurs during morphogenesis (unless acquired). Instead, it is considered to represent either normal peritrophoblastic flow of spiral arteries 8 or placental bed involution (or subinvolution if the vessels fail to obliterate) 9. This is supported by the common incidence of spontaneous resolution of enhanced myometrial vascularity, whereas a true arteriovenous malformation will not spontaneously regress.

It is impossible to distinguish enhanced myometrial vascularity from a true arteriovenous malformation on ultrasound 5

On greyscale ultrasound, there are anechoic, tortuous, tubular structures within the myometrium that may involve the endometrium. Echogenic intrauterine material in keeping with concurrent retained products of conception is commonly seen.

On color Doppler ultrasound, there is a mosaic turbulent pattern with multiple flow reversals. This demonstrates low impedance flow with a high peak systolic velocity (PSV) ≥20 cm/s and low arterial waveform pulsatility. It should be noted that while some authors consider a PSV >60 cm/s to be high risk 4,9,10, studies have shown that higher PSV values do not necessarily confer a greater hemorrhagic risk 1

MRI shows a bulky uterus with an ill-defined mass, disruption of the junctional zone (may be focal or diffuse) and abnormal serpentine uterine vessels seen as flow voids within the myometrium 10

Digital subtraction angiography (DSA) shows a hypervascular lesion without early venous filling. Conversely, a true uterine arteriovenous malformation will show a hypervascular mass with early venous filling 8,9.

If the patient is asymptomatic or has minimal vaginal bleeding, conservative management is advocated due to the transient nature of the phenomenon 1. This is done with serial ultrasounds and β-hCG monitoring to assess for retained products of conception. Occasionally medication such as gonadotropin-releasing hormone agonists, tranexamic acid, or uterotonic agents (e.g. misoprostol) may be used. Spontaneous resolution usually occurs after ~5 weeks (range 1 week to 6 months) 9. Resolution time has been found to be quicker with watchful waiting when compared to dilation and curettage 1.

Dilation and curettage in the setting of retained products of conception remains a viable alternative which often leads to resolution of the enhanced myometrial vascularity. There is no increased risk of hemorrhage when compared to dilation and curettage of retained products of conception without enhanced myometrial vascularity, except in the cases of cesarean scar and molar pregnancies 2,6,11.

In the setting of significant or prolonged vaginal bleeding, radiologically-guided uterine artery embolization is warranted, followed by more invasive surgical management (typically hysteroscopic electrosurgery, uterine/internal iliac artery ligation, or hysterectomy) as a last resort.

At the time of writing (c. 2022) no formal guidelines have been established and individualized therapy is therefore recommended.

The differential diagnosis for the sonographic appearance of a hypervascular lesion within the uterine myometrium with turbulent flow includes:

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Cases and figures

  • Case 1: EMV with spontaneous regression
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  • Case 2: likely EMV post-miscarriage
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  • Case 3: likely EMV post-D&C
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