Fetal vascular malperfusion, an update

Abstract

Fetal vascular malperfusion is the most recent term applied to a group of placental lesions indicating reduced or absent perfusion of the villous parenchyma by the fetus. The most common etiology of malperfusion is umbilical cord obstruction leading to stasis, ischemia, and in some cases thrombosis. Other contributing factors may include maternal diabetes, fetal cardiac insufficiency or hyperviscosity, and inherited or acquired thrombophilias. Severe or high grade fetal vascular malperfusion is an important risk factor for adverse pregnancy outcomes including fetal growth restriction, fetal CNS injury, and stillbirth. Overall recurrence risk for subsequent pregnancies is low.

Placentas From Women of Advanced Maternal Age

“…41 While the predominant risk factor is obstructed umbilical blood flow, there are other risk factors, including fetal hypercoagulability and processes causing vessel damage (such as from severe chronic villitis, acute chorioamnionitis with severe fetal inflammatory response, or meconium-associated myonecrosis). [50][51][52] The lesions described under the umbrella term of FVM include fetal vessel thrombosis, intramural fibrin deposition, avascular villi, villous stromal-vascular karyorrhexis, stem villous vessel obliteration, and vascular ectasia, and are further divided into high and low grade depending on both quantitative and qualitative measures. 41,50 FVM, particularly when high grade, has a strong association with poor fetal outcomes, which includes intrauterine fetal demise, intrauterine growth restriction, oligohydramnios, and cerebral events (cerebral palsy, stroke, hemorrhage).…”

“…[50][51][52] The lesions described under the umbrella term of FVM include fetal vessel thrombosis, intramural fibrin deposition, avascular villi, villous stromal-vascular karyorrhexis, stem villous vessel obliteration, and vascular ectasia, and are further divided into high and low grade depending on both quantitative and qualitative measures. 41,50 FVM, particularly when high grade, has a strong association with poor fetal outcomes, which includes intrauterine fetal demise, intrauterine growth restriction, oligohydramnios, and cerebral events (cerebral palsy, stroke, hemorrhage). 50,51 FVM was identified in 29.8% (50 of 168) of our overall AMA cases and 47.2% (17 of 36) of our pure AMA cases, which is higher than published reports noting an incidence of anywhere from approximately 1% to 20% of unselected placentas.…”

Placental assessment provides insight into mechanisms and timing of neonatal hypoxic-ischemic encephalopathy

“…The placental findings of FVM include extensive avascular villi, vascular obstructive lesions, necrotic fragments in villous stroma and vascular thrombi [1,5], often accompanied by abnormalities of the umbilical cord. Severe forms of FVM have been termed previously as "fetal thrombotic vasculopathy".…”

“…The disturbances of the umbilical cord may include intrinsic anatomic lesions (e.g., knots, coils, strictures), potentially obstructing anatomic lesions (e.g., placental insertion abnormalities), or potentially obstructing clinical conditions (e.g., prolapse, entanglements, oligohydramnios). The placental findings of FVM are considered to be secondary to chronic, partial or recurrent intermittent obstruction of umbilical blood flow, thereby leading to umbilical venous obstruction, and, as a consequence, venous congestion, stasis, thrombosis (in severe cases) and focal ischemia involving the distal portions of the villous tree [5]. The consequences for the fetus would be expected to include impaired fetal blood flow and oxygenation, and ultimately, cardiac insufficiency and compromised cerebral blood flow and oxygenation.…”

Gestational hyperglycemia on diet and medication: impact on placental pathology and pregnancy outcomes

“…Among the multitude of factors associated with FVM, maternal hyperglycemia plays a significant role. 24 Pregnancy per se is a thrombogenic state. When it is combined with maternal hyperglycemia (prothrombotic tendency) and hypercoiling of the cord (thereby causing vascular stasis and ischemia), it results in thrombosis in the foetal vascular tree, leading to foetal growth restriction and increased perinatal mortality and morbidity.…”