1

Placental Physiology
Placenta = autopsy of pregnancy Placental Exam Autopsy of pregnancy o What happened? o Will it happen again? Indications: o Maternal o Fetal o Placental Significant Pathology o Prematurity o Low Birth Weight Pathology Prematurity Ascending Infection o Think PID but with fetus o Intact Membranes o Ruptured Membranes o Endocervicitis o Breach membranes o Intramniotic replication o Maternal and fetal response Pregnancy induced hypertension o PIH o Pre-eclampsia o Eclampsia INTRAMNIOTIC INFECTION Pic1. Maternal inflamm Pic2. inflammation above Chorionic plate

Pic3. inflammation below Chorionic plate

Fetal Response: inflammatory infiltrate around umbilical vein NB: fetus has to be old enough to make mature PMNs for inflammatory response

Bugs and polys in amniotic sac Why do membranes rupture? Normally happens at term Two epithelia back-to-back

Membranes lay across cervical os Intact b/c Balance between synthesis and degradation of extracellular matris

Risks for Rupture Fetus has Hereditary collagen defects: Ehlers Danlos o Fetus affected b/c fetal tissue makes the placenta Nutritional defects: ascorbic acid deficiency; may be associated with cigarette smoking Short cervix, conization

What bacteria are they? group B streptococcus Mycoplasma Chlamydia Fusobacterium E.coli

2
Gonoccoccus enterococcus Both stds and colonizers of vagina or contaminants from perineum.

Result Maternal fever, can be bacteremic Fetus can eventually be infected but usually Labor commences and that works like draining an abscess Infection via Hematogenous Route Virus CMV, Parvovirus B19, Varicella Syphilis Toxoplasmosis Villitis Organisms reach intervillus space May breach trophoblast membrane Reach fetal vasculature o villus vascular destruction o fetal viremia VUE Unknown Etiology ? Unknown, undemonstrated viral infection Maternal T cells o Do fetal inflammatory cells migrate to the villus surface and generate cytokines to attract these cells? o Do fetal cells (? trophoblast) present Ags? Associated with IUGR

Lymphocytes hanging out around maternal blood in villus

Over time get in villus Cant recognize any fetal circulation- lots of inflammation Get poor nutrient exchange growth retarted pregnancy Intrauterine Growth Retardation Fetal growth plateaus Induced preterm delivery to enable baby to grow in healthier environment Pregnancy Induced Hypertension Clinical syndrome of hypertension >20 weeks of gestation With proteinuria and edema = pre-eclampsia With seizures = eclampsia Most effective treatment is ending pregnancy Etiology Placental ischemia Hypertension Disseminated intravascular coagulation

Decidua term for what endoemetrium becomes under first progesterone and then hCG Stromal cells become pulmp- glands become very inconspicuous Vsessels are converted from a little vessel with a muscular wall to large channels that are lined by endothelial cells but have no muscularis in the wall anymore and have no elastic fibers

Failure to Convert Blood Vessels Unassociated with aberrant invasion of the interstitium Defect of trophoblast, decidua, macrophages? Aberrant, vulnerable 3D vascular architecture

Early- lots of placenta very little baby By end- baby is 7x placenta Vessels get closer and closer to surface---space b/w moms blood and babys blood narrows What Can happen Accelerated Villous Maturation

Placenta is maxed out From lack of conversion Vessels may thrombose (Anti Pl, factor, V leiden, etc) Inflammation of vessel wall Thrombose INFARCT, necrosis of portion of vseesl supplised by that vessel Vessel wall necrotic- get LEAKAGE Can get abruption Other causes of Abruption Truama

Infarcts and Abruption

Infarct

4
Gross view of infarcts of varying ages Arrow points to area of abruption Patient with lupus Hemmorrhage pushes vessel wall aside Cessation of maternal blood flow See fibrin within the villi Death of villi from outside in Trophoblast dies first Cocaine use Not all are PREECLAMPSIA Dont alaways see things in placenta If comes from margin of placenta obstretrician will see bleeding but wont have direct impact on placenta itself If behind placenta lik ethse--- may not have external vaginal bleeding but baby may be in troublehaving blood loss that just isnt hsowing

Placentation in Twinning: Monozygous: Early division (dichorionic, diamniotic) Middle division (monochorionic, diamniotic) Later division (monochorionic, monoamniotic) Dizygous: (dichorionic, diamniotic) most common for IVF Monozygous Dizygous Complications of Twinning Premature delivery Monozygous associated abnormalities entangled cords in MoMo twin-twin transfusion

Monozygous- no chorion b/w the layers Get very thin see through dividing membrane

Lots of chorion in between Thicker membrane Cant see gloved hand b/w it Easier for ultrasonogrophaer to identify

SUMMARY Mainly associated with preterm delivery Unplanned o Rupture or infection Planned o Pre-eclampsia o Baby has interuterine growth retardation Then problems with prematurity

5
1. Premature rupture of membrane (PROM) At term: PROM Preterm: PPROM Prelonged preterm: PPPROM Membranes (2) layers: (slide against eachother rupture NL at birth) Amniotic epithelium (can be squamous tall columnar) BM Chorionic Mesoderm (Layers of CT + collagen) BM Chorionic/Trophoblastic epithelium (embedded in endometrium, harder to recognize these will be traveling into maternal basal plate) Sequelae of rupture: A. ascending infection (loss of barrier)

Most common infections: group B strep, Mycoplasma, Chlamydia, Fusobacterium, E.coli, Gonococcus, enterococcus NB: even with grossly intact membranes, infection can ascend endocervicitis reaches membranes, enter amniotic fluid maternal/fetal response Maternal Response: inflammatory cells extend from mesoderm up to amniotic epithelium

Result of infection: Maternal Sx (fever, sepsis?) Fetus may or may not be infected treated regardless Labor/delivery commences prematurely (works like draining an abcess) 2. Premature labor (Low Birth Weight): Causes: A. infection (see above) B. induced/iatrogenic C. abruption separation of placenta from the uterus prior to delivery -associated with trauma, pregnancy induced HTN (or pre-eclampsia), anti-phospholipids, lupus anticoagulant, thrombophelias (factorV laden, abNL protein C) *if occurs at margin, + vaginal bleeding (specimen looks NL to pathologist) *if occurs behind placenta, + pain, - vaginal bleeding trapped (hemorrhage/infarction can be seen by pathologist). Recall: Pregnancy Induced HTN May be caused by improper transformation of spiral arteries (associated w/ placental ischemia? DIC?) NL spiral arteries in endometrium are Thin-walled (tips are shed monthly) w/ musculature. In first 20wks gestation, trophoblasts transform them into high capacity, low pressure system with no musculature. (endothelium, with trophoblasts surrounding vessel instead of musculature). NL villi: 1st trimester - stroma:vessels -cyto & syncytio both present - distance b/w maternal & fetal circulation 2nd trimester -lose cytotrophoblast -lower stroma:vessels (#vessels) 3rd trimester -trophoblastic layer very thin -lots of fetal vessels -maternal & fetal circulation in close proximity Pathology: A. Thrombosis of these spiral vessels (pre- or post- conversion). [ANA, anti-PL, pre-eclampsia]

6
Result: infarcts (from trophoblast, in), coagulative necrosis. Nb: infarcts are not repaired in placenta no fibrosis/liquefaction. B. vessels that dont convert Result: small, ischemic placenta, fetal villous maturation is accelerated (to try and compensate for poor maternal circulation). Villous maturation will max out, placental size will max out, and fetus will cease to grow. C. vessel walls that become necrotic fibrinoid necrosis (bright pink blobs, stains like fibrin) w atherosis (foamy m) Result: can rupture vessels abruption D. Aberrant invasion Often around scarred areas, will get aberrant invasion. Adherent area of placenta, and placenta will not deliver. Accreta (does not invade muscular) increta (invades muscular) percreta (thru uterus) Causes of intrauterine growth retardation -improper vessel conversion (See B. above) -Villitis -95% are Villitis of unknown etiology (VUE), no known infection (perhaps an undemonstrated viral infection?) -involve maternal Tcells attracted to villi -alters function of membranes, damages fetal circulation growth retardation -Associated with:

Virus (CMV, Parvovirus B19, Varicella)

Syphilis Toxoplasmosis