Surface Chorionic Vasculitis

Today I had a case of what appears to be insudation of protein or possibly mural fibrin in the superficial chorionic vessels with acute inflammation. The lesion has some resemblance to acute atherosis or TTP. This placenta is from a 25 week, 825 g birth weight infant with purulent chorioamnionitis, but not very intense three vessel funisitis or chorionic vasculitis, at least in terms of neutrophil density. The membranes show a marked thickening of the amnion connective tissue with neutrophils and neutrophil debris.
This vessel lesion is very distinctive, although it probably falls under the SPP category of fetal inflammatory response with thrombus. There must be specific factors causing this pattern of vascular injury. The localization suggests a direct effect either from surrounding inflammatory cells, or even amniotic fluid components. Serum factors may be detectable in umbilical vein blood. Serum factors injuring this vessel (one of several seen in this placenta) might be capable of causing similar vascular injury in the fetus, especially if the umbilical venous blood adjacent to the lesion is going directly to the fetal brain via the foramen ovale. Dr. Redline and colleagues were able to demonstrate an association of chorionic non-occlusive thrombi with cerebral palsy and other neurologic impairment1. I could not tell from this article, since it was retrospective based on neurologic impairment, the predictive value of thrombi in the chorionic vessels for neurologic impairment. I am willing to bet it is high.
The Society for Pediatric Pathology created provisional guidelines for staging and grading chorioamnionitis2. Dr. Redline led the group based on his experience and publications investigating chorioamnionitis in very low birth weight infants. These guidelines were meant to be validated through further research. The problems with obtaining research and HIPPA protocols for follow-up are daunting, and I know I shall not pursue this case. However, these advanced inflammatory placental lesions are still an area in need of better clinical pathological correlation.


1. Redline RW, Wilson-Costello D, Borawski E, Fanaroff AA, Hack M. Placental lesions associated with neurologic impairment and cerebral palsy in very low-birth-weight infants. Arch Pathol Lab Med 1998;122(12):1091-8.
2. Redline RW, Faye-Petersen O, Heller D, Qureshi F, Savell V, Vogler C. Amniotic Infection Syndrome: Nosology and Reproducibility of Placental Reaction Patterns. Pediatr Dev Pathol 2003.

Acute Atherosis

Acute atherosis not in preeclampsia.

I had a case today, and periodically have had other cases, of the unexpected finding of acute atherosis in the spiral arteries in the placental membranes. This was a case of preterm premature rupture of membranes, and the infant was borderline small but there was no evidence of preeclampsia in the electronic medical record. I am puzzled as to what this finding means if anything to the future of the child or mother.

What is acute atherosis?

The lesion is most often found in pre-eclampsia but has been reported in unexplained intrauterine growth retardation and in a case of SLE. Acute atherosis appears to be a lesion of insudation of serum proteins including lipoproteins (hence foam cells) into the spiral artery media. Some have likened the lesion to that caused by angiotensin There are high concentrations of molecules in the renin angiotensin system in the decidua. However, injury to and serum leakage through the endothelium is perhaps a more plausible mechanism given the wide spread endothelial injury in pre-eclampsia. An understanding of the lesion should answer two critical questions: 1) why does the lesion occur only in spiral arteries, and 2) why is the lesion present in only some cases of preeclampsia?
Even large studies of maternal arteries have not found acute atherosis in other organs. It is not for lack of looking, e.g. 677 maternal autopsies reported by Sheehan and Lynch1. Perhaps it has something to do with the hormonal responsiveness of these vessels that constrict with menstruation, as elegantly demonstrated in endometrial transplants into the anterior chamber of monkey eyes. At the least, the arteries are unusual in that they shed with each menstruation and are surrounded in pregnancy by decidual cells.
Acute atherosis is present in only a minority of patients with preeclampsia. This is unlikely to be a sampling error, although not all membrane samples contain many or even any spiral arteries. I presented an abstract at our MAPS meeting showing little gain in diagnosis with 4 samples compared to one sample of membrane. Subsequently Yasser Morgan and I demonstrated that we could identify acute atherosis using a dissecting scope of the membranes stretched over a white card. Even with this technique spiral artery lesions may not be present. While a single sample of membranes may miss some cases of acute atherosis, the evidence suggests that in most cases the lesion is not really present. Perhaps acute atherosis is a marker for yet another preeclampsia associated angiopathic protein, like sFlt1 and endoglin.
Note to pathologists: A colleague tells me he never sees it! I suggest to novice pathologists that they should scan the entire membrane slide at low power for vascular lesions as part of the routine approach to placental slides. With experience acute atherosis will stick out like a pink highlighted text. I make the diagnosis if the bright pink fibrinoid of the media is present, and do not require foam cells. The diagnosis is more difficult in the basal decidua because most spiral arteries have been destroyed by trophoblastic invasion and are only fibrin lined shells lined with trophoblast. However, distinct acute atherosis does occur in the basal decidua, likely in vessels not invaded by tropphoblast.


1. Sheehan HL, Lynch JB. Pathology of Toxaemia of Pregnancy. Baltimore: The William and Wilkins Company; 1973.