Placental Pathology
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SP-05-_______________________                                       PATIENT’S NAME: _________________________           

RESIDENT: _________________                                          ATTENDING: ______________________________

DIAGNOSIS:

PLACENTA, CLINICALLY ________ WEEKS, DELIVERY:

VERY SMALL / HEAVY / IMMATURE / MATURE PLACENTA, __________ GRAMS (CORRECTED)

WEIGHT BETWEEN  ______TH AND ______TH PERCENTILE FOR GESTATIONAL AGE

ACUTE CHORIOAMNIONITIS

FUNISITIS, MONOVASCULAR  /  BIVASCULAR  /  TRIVASCULAR

CHORIONIC VASCULITIS

FETAL STEM VILLOUS FIBRIN THROMBI

VILLOUS EDEMA

ACUTE / CHRONIC DECIDUITIS

CHRONIC VILLITIS.  NO PATHOGENS IDENTIFIED

PIGMENT-LADEN MACROPHAGES IN EXTRAPLACENTAL MEMBRANES  /  WHARTON’S JELLY

SHORT, (?) INCOMPLETE UMBILICAL CORD, __________ CMS

EXCESSIVELY LONG UMBILICAL CORD, __________ CMS

AMNION NODOSUM

DECIDUAL VASCULOPATHY,  MEDIAL HYPERTROPHY TYPE /  ACUTE ATHEROSIS TYPE

INCREASED VILLOUS CELLULARITY _______________________________________

FETAL ARTERY THROMBOSIS          _______________________________________

INFARCT(S)                                   _______________________________________

ACCELERATED VILLOUS MATURATION _____________________________________

INCREASED VILLOUS VASCULARITY     _____________________________________

INTERVILLOUS THROMBUS/THROMBI   ____________________________________

RETROPLACENTAL HEMORRHAGE(S)    ____________________________________

PLACENTA ACCRETA

INCREASED FETAL NUCLEATED ERYTHROCYTES

SICKLED MATERNAL ERYTHROCYTES

SEE COMMENT (S) 

●  Comment: Histologic features are compatible with ascending amniotic fluid infection / placental abruption / pre-eclampsia.

●  Comment: In some instances, chronic villitis is associated with congenital infections by the following organisms: Toxoplasma gondii, Rubella virus, Cytomegalovirus, Herpes simplex virus (TORCH infections), Parvovirus, Treponema pallidum, Mycobacterium tuberculosis, Histoplasma, Varicella zoster virus, and Enteroviruses, including Coxsackievirus, among others.  In cases in which an infectious cause can not be demonstrated, the possibility of a maternally-derived immune reaction against the placenta has been postulated.  Clinicopathologic correlation and serum antibody titers are recommended if clinically indicated.  Ref: Am J Pathol. 1993 Aug;143(2):473-9.

●  Comment: Increased fetal nucleated red blood cells may be associated with congenital anemia due to a variety of etiologies including congenital infection, fetal maternal hemorrhage, congenital abnormalities, blood group incompatibilities, Rh disease, and placental abruptioin, among others.  Clinicopathologic correlation is recommended.  Ref: Arch Dis Child Fetal Neonatal Ed. 2001 May;84(3):F211-5.

●  Comment: Maternal diabetes has been associated with placental abnormalities, including placentomegaly, chorangiosis, and immature, edematous villi, as well as cord abnormalities including increased cord diameter and single umbilical artery.  Ref: Placenta. 2003 Sep-Oct;24(8-9):819-25.

●  Comment: Septic intervillous thrombi and/or acute villitis have been associated with in utero infections with Listeria monocytogenes, among others.  Ref: NEJM 1997;336(20):1439-46.

●  Comment: Gross and histologic features of a small, growth-restricted placenta, accelerated villous maturation, infarcts, and decidual vasculopathy(acute atherosis) are characteristic of pre-eclampsia. Refs: Indian J Pathol Microbiol. 1990 Jan;33(1):11-6.  Obstet Gynecol. 1964 Sep;24:350-6.

●  Comment: Fetal inflammatory response exceeds maternal response, a situation common to beta-Streptococcal infections, among others.

●  Comment: Early funisitis in the absence of other histologic evidence of ascending amniotic fluid infection (acute chorioamnionitis, chorionic vasculitis, etc.) may be seen with intermittent umbilical cord compression.

●  Comment: Fetal vascular obstruction (fetal artery thrombosis, hemorrhagic endovasculitis) has been associated with maternal diabetes, maternal thrombophilia, chorioamnionitis, and umbilical cord abnormalities.  When extensive, fetal vascular obstruction has been associated with fetal growth restriction, neurologic impairment (including cerebral palsy), vascular compromise, and stillbirth.  Refs: Hum Pathol 1999 Jul;30(7):759-69.  Hum Pathol. 1995 Jan;26(1):80-5.

●  Comment: Short umbilical cords (variably defined as 35-40 cm) have been associated with decreased fetal in utero movement (as may be seen with amniotic bands, oligohydramnios, body wall defects, and fetal neuromuscular disorders, among others), low Apgar scores, small for gestational age, and psychomotor abnormalities.  Clinicopathologic correlation with length of umbilical cord left on the baby and any used for blood gas analysis is recommended to evaluate overall cord length.  Refs: Obstet Gynecol. 2004 Jan;103(1):119-27.  J Pediatr. 1985 Aug;107(2):278-81.  Obstet Gynecol. 1981 Apr;57(4):450-2.

●  Comment: Excessively long umbilical cords (>80 cm) have been associated with an increased risk of nuchal cord, umbilical cord prolapse, increased fetal nucleated red blood cells, chorangiosis, fetal vascular thrombi, and meconium stained membranes.  Ref: Pediatr Dev Pathol. 2001 Mar-Apr;4(2):144-53.

●  Comment: Single umbilical artery is an uncommon cord abnormality which had been associated with congenital abnormalities (particularly affecting the cardiac and renal systems), increased perinatal mortality, prematurity and low birth weight.  Refs: Genet Med. 2004 Jan-Feb;6(1):54-7.  Perspect Pediatr Pathol. 1984 Wintre;8(4):345-78.

●  Comment: Multiple intervillous thrombi suggest the possibility of fetomaternal hemorrhage and have been associated with fetal anemia, fetal thrombocytopenia, and maternal sensitization.  A Kleihauer-Betke test is recommended if clinically indicated.  Ref: J Obstet Gynaecol Br Commonw. 1964 Jun;71:379-87.

●  Placenta reviewed at Placental Conference by Drs. Lage, Caplan, Cady, McEvoy, and __________________________.

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Last modified: 03/05/06