Placental Chorangiosis

A placenta from a 39-year-old woman, gravida 2, para 0, with pre-eclampsia was received for routine pathologic examination. She was admitted to the hospital at term in labor. She presented with facial and ankle edema and elevated blood pressure with diastolic pressure in the 90s. She also had proteinuria of +1.

Labor was induced with Pitocin, but fetal monitoring showed tachycardia with decreased variability. The patient was taken to the operating room for cesarean section. A healthy baby boy was delivered; he weighed 3050 g and had an Apgar score of 9 at 1 minute.

The placenta weighed 625 g and was grossly unremarkable. Microscopically it showed an increase in the number of vessels in the chorionic villi, a characteristic finding of chorangiosis.

Normal chorionic villi should contain no more than 5 vascular channels, even when the same vessel is present in more than 1 plane of section. The diagnostic criteria of chorangiosis were established by Altshuler1 in 1984 as the presence of a minimum of 10 villi, each with 10 or more vascular channels, in 10 or more areas of 3 or more random, noninfarcted placental areas when using a ×10 ocular (Figure, original magnification ×10). Chorangiosis should be differentiated from congestion, in which vasculature is numerically normal, and from tissue ischemia with shrinkage of villi. The criteria to evaluate the severity of this process include determining the number of vessels within each villus and the placental area throughout which the vasculature is seen.1 

Chorangiosis is a placental change that has not been extensively studied. Its etiology is still not clear, but it is believed to result from long-standing placental hypoperfusion or low-grade tissue hypoxemia. This also occurs in pre-eclampsia, a condition in which placental tissue hypoxia causes villous capillary endothelial cell proliferation and capillary hypervascularity. We corroborate the association of pre-eclampsia with chorangiosis in our case.2 

Numerous other conditions have been suggested as having an etiologic role in the development of chorangiosis, including maternal, fetal, and placental conditions.1 The associated maternal conditions include pre-eclampsia/eclampsia, as already mentioned; diabetes mellitus (placentomegaly is especially frequent among placentas with chorangiosis); drug ingestion; and urinary tract infection. Placental conditions that have been associated with chorangiosis include umbilical cord anomalies, single umbilical artery, abruptio placentae, placenta previa, chorangioma, amnion nodosum, and villitis (rubella virus, cytomegalovirus, syphilis, and Bartonella sp are known to infect and induce proliferation of the endothelial cells). When these diseases and viruses are present, an abnormal placenta could decompensate acutely, leading to a catastrophic outcome.3 The fetal factors most commonly associated with chorangiosis are the presence of major congenital anomalies and Apgar scores of less than 5.

The incidence of chorangiosis is higher in women living in high altitudes, and thus a hypoxic stimulus may well lead to an excessive villous capillary and to connective tissue proliferative activity, perhaps via growth factors such as vascular endothelial.

Chorangiosis has been associated with increased perinatal morbidity and mortality, though the ultimate mechanism by which chorangiosis is involved in adverse perinatal outcomes is unknown.

In conclusion, the cause of chorangiosis is still unknown; the interaction of maternal, placental, and fetal factors may combine to produce this pathologic change. Whatever its cause, it should be considered as a placental sign of potential clinical significance.