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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 proteinuria /pro·tein·uria/ (-ur´e-ah) an excess of serum proteins in the urine, as in renal disease or after strenuous exercise.proteinu´ric

pro·tein·u·ri·a
n.
1.
 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 Altshuler[1] in 1984 as the presence of a minimum of 10 villi villi: see digestive system. , each with 10 or more vascular channels, in 10 or more areas of 3 or more random, noninfarcted placental areas when using a X10 ocular (Figure, original magnification X10). Chorangiosis should be differentiated from congestion The condition of a network when there is not enough bandwidth to support the current traffic load.

congestion - When the offered load of a data communication path exceeds the capacity.
, in which vasculature vasculature /vas·cu·la·ture/ (vas´ku-lah-chur)
1. circulatory system.

2. any part of the circulatory system.


vas·cu·la·ture
n.
 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 villus /vil·lus/ (vil´us) pl. vil´li   [L.] a small vascular process or protrusion, especially from the free surface of a membrane.

arachnoid villi 
1.
 and the placental area throughout which the vasculature is seen.[1]

[ILLUSTRATION OMITTED]

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 hypoxemia /hy·pox·emia/ (hi?pok-sem´e-ah) deficient oxygenation of the blood.

hy·pox·e·mi·a
n.
Insufficient oxygenation of arterial blood.
. This also occurs in pre-eclampsia, a condition in which placental tissue hypoxia causes villous villous /vil·lous/ (vil´us) villose.

vil·lous or vil·lose
adj.
Of, relating to, resembling, or covered with villi.



villous

pertaining to or emanating from villi.
 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 eclampsia (ĭklămp`sēə), term applied to toxic complications that can occur late in pregnancy. Toxemia of pregnancy occurs in 10% to 20% of pregnant women; symptoms include headache, vertigo, visual disturbances, vomiting, , as already mentioned; diabetes mellitus (placentomegaly is especially frequent among placentas with chorangiosis); drug ingestion; and urinary tract infection urinary tract infection (UTI),
n infection in one or more of the structures that make up the urinary system. Occurs more often in women and is most commonly caused by bacteria.
. 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 decompensate,
n the development or worsening of a mental disorder.
 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 Morbidity and Mortality can refer to:
  • Morbidity & Mortality, a term used in medicine
  • Morbidity and Mortality Weekly Report, a medical publication
See also
  • Morbidity, a medical term
  • Mortality, a medical term
, 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.

References

[1.] Altshuler G. Chorangiosis: an important placental sign of neonatal morbidity and mortality. Arch Pathol Lab Med. 1984;108:71-74.

[2.] Altshuler G. Role of the placenta in perinatal pathology. Ped Pathol Lab Med. 1996;16:207-223.

[3.] Benirschke K, Franciosi R. Placental pathology casebook A printed compilation of judicial decisions illustrating the application of particular principles of a specific field of law, such as torts, that is used in Legal Education to teach students under the Case Method system. . J Perinatol. 1999; 19:393-394.

Accepted for publication March 12, 2001.

From the Arkadi M. Rywlin Department of Pathology and Laboratory Medicine, Mount Sinai Medical Center, Miami Beach, Fla.

Reprints: Margarita M. De La Ossa, MD, Mount Sinai Medical Center, Department of Pathology, 4300 Alton Rd, Blum Bldg, Room 201, Miami Beach, FL 33140 (e-mail: mdelaossa@hotmail.com).
COPYRIGHT 2001 College of American Pathologists
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2001 Gale, Cengage Learning. All rights reserved.

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Author:De La Ossa, Margarita M.; Cabello-Inchausti, Beria; Robinson, Morton J.
Publication:Archives of Pathology & Laboratory Medicine
Article Type:Brief Article
Geographic Code:1USA
Date:Sep 1, 2001
Words:652
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