Acute & Chronic Villitis (VUE or DSV)
Acute villitis implies foci of numerous
polys affecting villi and tends to indicate E. coli, listeria,
or Campylobacter infection.
Chronic villitis can be seen as
a very minor, inconsequential finding or rarely, with a more important
degree of villous involvement.
diffuse sclerosing villitis (DSV...TORCH
villitis): When essentially all villi are involved and
include a prominent histiocytic component, the variety of
chronic villitis is DSV (diffuse-sclerosing villitis),
DSV implying an infectious etiology (TORCH and luetic infections).
Lymphoplasmacytic cell infiltration suggests lues, CMV, herpes,
or Rubella1, abundant plasma cells most
likely CMV7. The mother tends to present
somewhat ill, possibly with IUGR, IUFD, or evidence of NIHF.
villitis of undetermined etiology (VUE): The
other, more common variety of chronic villitis is villitis
of undetermined etiology (VUE) which is marked by a
sub-total involvement of villi, >10% of villi being affected
signifying a severe degree of involvement. A chronic villitis
placenta does not usually look abnormal on casual gross inspection.
Some feel7 that the VUE reaction reflects
a graft-versus-host reaction with the inflammatory response
halting the maternal reaction against fetal antigens at the
level of the placenta. Mother tends not to be ill; and VUE
has been associated with recurrent reproductive failure, as well as abnormal nonstress testing18, IUGR18,
and mid-trimester elevations of maternal AFP18. Villi infiltrated by activated maternal T lymphocytes18. Vue with vasculitis/perivasculitis, fetal vascular occlusion, and downstream avascular terminal villi (obliterative fetal vasculopathy)18.
Future pregnancies (obstetrical view):
When there is a prominent degree of involvement,
there is an uncertain but known risk of VUE recurrence in subsequent
pregnancies7. Assuming that any treatable TORCH/luetic
infection was treated and resolved in the mother, recurrence of
the DSV variety is said to be rare.
Sequelae in the newborn (pediatric view):
In the case of the VUE variety, there is a relatively
infrequent association with TORCH/luetic etiology; therefore, any
newborn sequelae would be (as in the DSV variety) relative to any
actual such infection. If the VUE is extremely prominent and with
evidence of chronic vascular insufficiency (prominent villous edema;
significant erythroblastosis; newborn polycythemia) or association
with additional lesions suggesting subacute or chronic vascular
compromise, then sequelae are possible. Since IUGR can be seen
in both VUE and DSV varieties, when IUGR is present, possible sequelae
are at least related to the fact of IUGR.
If the newborn appears to have neurologic injury,
then management is by standard methods. If there is no apparent
abnormality, then care should be taken (all cases DSV; severe cases
VUE) that the baby is seen at typical and standard times throughout
childhood development in order to detect any milestone delays in
order to allow early corrective intervention should delays be encountered6.
It is too premature in our understanding of possible
sequelae to actually routinely discuss such risks with parents.
Ervin B. Shaw, M.D.
August 15, 1994
Spark RP, The Placenta: the Rebirth of the Afterbirth, a Critical Assessment & Clinicopathologic Correlation Lecture, AAPA workshop handout, September 2003 Phoenix meeting.
Naeye, Richard L., "Progress in Pathology:
Functionally Important Disorders of the Placenta, Umbilical Cord, and Fetal
Membranes", Human Pathology 18(7):680-691, 7/87.
Althabe, O., Labarrere, C., "Chronic Villitis of
Unknown Etiology and the Uterine Growth-Retarded Infants of Normal and Low
Ponderal Index", Placenta 6:369; 1985 (referred to in reference #2).
Sander, C. Maureen, Personal Communication Letter
to Dr. Shaw, 2 pgs., 6/8/94.
Altshuler, Geoffrey, "Placenta Within the
Medico-Legal Imperative", Archives of Pathology and Laboratory Medicine,
Salafia, Carolyn M., "Gross and Microscopic
Diagnosis of the Placenta: How to Do It and Its Clinical Revelance", American
Society of Clinical Pathologists Teleconference Series 1929, Session I,
Syllabus, pgs. 1-14; 9/14/90.
Redline, Raymond W., "Practical Placental
Pathology: Identifying the Clinically Important Lesions", American Society of
Clinical Pathologists, Orlando National Meeting, Workshop, Syllabus, pgs. 2-47;
Sander, C.M., Kinnane, L., and Stevens, N.G.,
"Hemorrhagic Endovasculitis of the Placenta: A Clinical Pathologic Entity
Associated With Adverse Pregnancy Outcome", Comprehensive Therapy, 11(5):66-74;
"Preventing Prenatal Injuries: An Update, A Manual
Prepared on Behalf of the Risk Management Committee of the Doctors Company, 32
Sander, C.M., manuscript in preparation 8/93
through 7/94, "What's New in Placental Pathology", scheduled for publication in
Pathology Annual, spring of 1995.
Stoeckmann, A., "Placental Examination As a Risk
Management Tool", Journal of Health Care Risk Management, pgs, 9-14, Winter
Naeye, Richard L., "Do Placental Weights Have
Clinical Significance?", Human Pathology, 18(4):387-391; 4/87.
Clements, W., malpractice series part 4, "The Most
Common Causes of Lawsuits and How You Can Protect Yourself. This week:
Dangerous Deliveries", American Medical News; 1 Aug '94.
Kaplan, Cynthia, "Specific Problem Areas in
Placental Pathology, "Practical Reviews in Pathology (audio-series and
subsequent ASCP workshops), 17(8), Dec. 1992.
MacPherson, Trevor, "Fact and Fancy: What Can We
Really Tell From the Placenta?", Arch. of Path. and Lab Med., 115(7):672-681,
Kurman, R.J. (editor), Blaustein's Pathology of the
Female Genital Tract, 4th Ed., 1994 [Placenta Chpt. 23, Deborah J. Gersell and
Fred T. Kraus].
Kraus, Fred T., Guest Editor, "Controversies and
Advances in Placental Pathology", Seminars in Diagnostic Pathology, 10(3):1-283;
- Redline RW, Severe fetal placental vascular lesions in term infants with neurological impairment, Am. J. Obstetrics & Gynec. 192:452-457, 2005.
|(file produced August 5, 1994; posted August 2002; latest addition
9 August 2006)