Placenta

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The placenta feeds the developing baby, breathes for it and disposes of its waste.

Clinical

Examination of the placenta

  • Most placentas are not examined by a pathologist.

Indications for exam by pathology

Some indications for exam by a pathologist:

  • Abnormalities in the:
    1. Fetus:
      • Bad fetal outcome.
      • Suspected or known congenital abnormalities or chromosomal abnormalities.
    2. Mother:
      • Infection/suspected infection.
      • Pre-term labour.
      • Maternal disease (e.g. SLE, coagulopathy).
      • Complicated pregnancy (preclampsia, pregnancy induced hypertension, gestational diabetes).
    3. Placenta:
      • Unusual gross characteristics.[1]

A more detailed list is given by Hargitai et al.[2] and Chang.[3]

Most common

Most common reasons for submitting a placenta to pathology:[4]

  1. Prematurity.
  2. PROM / possible chorioamnionitis.
  3. Multiple gestation.

Bleeding in late pregnancy

DDx of bleeding in late pregnancy:

  • Placental abruption (most common).
  • Placenta previa.
  • Vasa previa (fetus losing blood).

Clinical screening tests

  • PAPP-A - low values seen in aneuploidy.[5]
Main article: Pregnancy

Normal histology

Villi

Main article: Chorionic villi

This is dealt with in a separate article that also covers the types of trophoblast (cytotrophoblast, syncytiotrophoblast, intermediate trophoblast).

Cord

Omphalomesenteric duct remnant

  • AKA vitelline duct.
  • Benign embryologic remnant.

Features:

  • Duct with benign looking cuboidal epithelium.

Allantoic duct remnant

  • Benign embryologic remnant.

Features:

  • Duct with benign looking flat epithelium.

Vitelline artery remnant

Features:

  • Small artery in the cord.

Membranes

Fetus to mother:

  • Amnion - thin layer: one cell layer, basement membrane, connective tissue.
  • Cleft - artifactual - empty space.
  • Chorion - vascular.
  • Decidua (maternal tissue) - may contain obsolete chorionic villi; place to look for hypertensive changes.

Amnion

General:

  • Next to fetus, surrounds amniotic fluid, avascular.

Characteristics:

  • Characterized by a single layer of cells.[6]
    • Cuboidal/squamoid shape.
    • Eosinophilic cytoplasm.
    • Central nucleus.
  • Squamous metaplasia may be seen at cord insertion.
  • Basement membrane.
  • 'Compact layer'.[6]
  • 'Fibroblastic layer'.[6]

Chorion

General:

  • Surrounds amnion.

Characteristics:

  • Layers:[7]
    • 'Reticular layer' - cellular (inner aspect).
    • 'Pseudo-basemement membrane'.
    • 'Outer trophoblastic layer'.
  • Has blood vessels.
  • Opposed to "trophoblastic X cells" on side opposite of amnion.[6]
    • Beneath of the "trophoblastic X cells" is decidua (mnemonic NEW = nucleus central, eosinophilic, well-defined cell border), which is maternal tissue.

Common terms

  • Chorionic plate - fetal aspect of placenta.
  • Basal plate - maternal aspect of placenta.
    • Has extravillous trophoblast.
    • Place to look for maternal vessels.

Grossing

This is often very quick. The gross is quite important, as some things cannot be diagnosed microscopically.

General

  • Dimensions:
    • Disc.
    • Length of cord, diameter of cord.
    • Accessory lobes - dimensions.
      • Two lobes of equal size + cord arises in between = bilobate placenta.
  • Mass (weight).
    • Should be done 'trimmed' (cord cut-off, membrane cut-off).
    • Should be done when placenta is "fresh", i.e. not fixed -- as mass tables are based on fresh state.
  • Umbilical cord
    • Attachment.
      • Location: central, eccentric, marginal.
        • Marginal attachment assoc. with hypertension[8]
      • Membranous or velamentous (veil-like) insertion.
        • Vessels separate/branch prior to reaching placental disc.
      • Furcate insertion - vessel run on fetal surface (more exposed to trauma).
    • Knots (false vs. true).
      • False knots are nothing to worry about -- look like a knot but aren't really one.
    • Twisting/coiling - 1-3 coils/10 cm is normal.
    • Number of vessels.
      • Normal: 2 arteries, 1 vein.
  • Membranes - shiny & translucent - normal (green, opaque/dull - chorioamnionitis).
    • Attachment: marginal (normal), circummarginate (inside edge), circumvallated (folding on self).
    • Site of rupture - if obvious; low point of rupture suggests low-lying placenta.
  • Placental disc.
    • Fetal surface - normal is shinny.
      • Dull in chorioamnionitis.
    • Maternal surface
      • Are the cotyledons intact?
      • Adherent clot?
    • Parenchyma - after sectioning:
      • White vs. red nodules.

Notes:

  • Parenchymal nodules - a brief DDx:
    • White: infarct (chronic), thrombi, chorangioma, perivillous fibrin deposition.
    • Red: infarct (acute), thrombi.

Sections

  1. Cord two sections.
  2. Membranes (rolled), two rolls or more.[9]
  3. Cord at insertion + disc.
  4. Placenta - full thickness (maternal and fetal surface).
    • Sections should not be taken at the margin of the disc.

Placental membranes

Appearance:[10]

Placental mass

It is considered routine to obtain a mass for the placenta. This is usually done when the placenta is fresh and with the membranes and cord trimmed, as most tables of placental mass were created with these parameters.

Placental mass by gestational age:[12]

Gest. Age/Percentile 25% 50% 75%
32 weeks 275 g 318 g 377 g
36 weeks 369 g 440 g 508 g
40 weeks 440 g 501 g 572 g

Linear regression - placental mass-gestational age

Based on the table in the AFIP book[13] I generated the following regression lines:

50% 10% 90%
slope (g/week) 21.58088235 19.70588235 25.40196078
y-intercept (g) -357.4558824 -397.2352941 -366.7254902
Pearson (r) 0.988670724 0.988268672 0.982206408

placental mass = slope x gestational age + intercept

What to remember...

Extrapolated from the linear regression (see above):

  • 50% at term = 500 grams.
  • 50% at 26 weeks = 200 grams.
  • The change in mass/week is approximately linear and equal to 300 grams / 14 weeks ~ 20 grams/week.
  • The spread in mass between 10% and 90%, crudely estimated, is 200 grams (for GA=26-40).

Notes:

  • Is it required?
    • Sebire and Fox have advocated abandoning the practise of obtaining a placental mass, due to the large number of uncontrolled variables inherent in these measures. Instead, they have advocated using mushy descriptors such as "small", "average" and "large", which require experience in examining the organ.[14]
      • In the context of quality, a measure (even if somewhat flawed), is almost certainly more reproducible than arbitrary descriptors which require experience and a continuing case volume to calibrate.

Overview of placental pathology

Approach

The pathology of the placenta is diverse and is not easy to group.

It terms of remembering things. It is probably easiest to take a combined anatomical, etiologic and morphologic approach.

Anatomical basis:

  • Cord.
  • Membranes.
  • Disc.

Etiologic:

  • Congential.
  • Infectious.
  • Neoplastic.
  • Endocrine.
  • Trauma.
  • Vascular.
  • Degenerative.
  • Autoimmune.
  • Toxic.
  • Idiopathic.

Compartmental:

  • Vasculature.
  • Membranes.
  • Parenchyma:
    • Maternal part (decidua).
    • Fetal part (villi, cord).

Common entities/diagnoses

  • Normal.
  • Chorioamnionitis.
  • Placental abruption.
  • Meconium.
  • Hypertensive changes.

Sign-out

What should be commented on...

  • Placenta:
    • Maturity of villi (2nd or 3rd trimester).
    • Infarction?
      • Subchorionic less important than maternal aspect.
      • Peripheral aspect of placental disc less important than central region of disc.
    • Blood vessels.
      • Maternal.
      • Fetal.
  • Membranes.
    • Membranitis?
    • Chorioamnionitis?
  • Cord:
    • 3 vessel?
    • Vasculitis/inflammation?

Mnemonic: chorio, cord, vessels, villi (maturity, infarction).

Cord pathology

  • Two vessel cord.
  • Hypercoiling/Hypocoiling.
  • Abnormal insertion.
  • Cord knots (true vs. false).
  • Strictures.
  • Hematoma.
  • Hemangioma.
  • Benign cyst.

Two vessel cord

  • AKA single umbilical artery.

Associations

  • Associated with congenital abnormalities, esp. cardiac - key point.[15]
    • Thought to be an acquired defect (as prevalence is lower in early in gestation).
  • May be seen in association of other cord abnormalities (e.g. marginal insertion, velamentous insertion).
  • In apparently well (liveborn) infants it is associated with (occult) renal abnormalities, specifically vesico-ureteric reflux; there is no evidence for other abnormalities.[16]
  • Associated with maternal diabetes.[17]

Image:

Insertion

Marginal insertion

Definition:

  • The umbilical cord is attached to the placental disc at its margin.

Prevalence:

  • Approximately 12% of placentas.[15]

Relevance:

  • None according to WMSP.[15]
    • In theory, the cord, dependent on its relation to the internal os, is at greater risk of injury (leading to vasa previa) and compression (fetal hypoxia). A retrospective study found cord position in relation to the internal os is predictive for vasa previa.[19]

Velamentous insertion

Definition:

  • The umbilical cord inserts into the fetal membranes.[15]
    • The vessels are not protected by Wharton's jelly.
      • Wharton's jelly = the connective tissue surrounding the vessels in the cord.

Details:[15]

  • 3/4 of the time the vessel also branch; in the remaining 1/4 the vessels stay together.

Relevance:

  • Increased risk of vasa previa.[19]

Knots

General

Gross

Work-up:[21]

  • Diameter measures and colour on both sides of the knot.
  • Knot should be untied to assess for deformation of Wharton's jelly.
  • Sections from both sides of the knot - to look for thrombi.

Note:

  • False knots (large diameter - focally) are common - they cannot be untied.

Microscopic

Features:

  • +/-Thrombi.
    • Fibrin deposition.
  • +/-Lines of Zahn.

Images:

Coiling

  • Hypo- and hypercoiling are both considered problematic.[15]
    • Normal: 1-3 coils/10 cm.[22]
  • Associated with cord stricture, which is usu. at the fetal end of the cord.[23]

Notes:

  • There is little uniformity in how coiling is assessed in the medical literature - though 10% and 90% are considered the cut-points for normal.[24]
    • What are the 10% and 90% cut-points? They are not given in WMSP. UT access to a journal article[25] that might have it is screwed-up.

Cord hematoma

Features:[23]

  • Rare ~ 1/5500.
  • Mortality ~50% is severe.

Image: Hematoma (flylib.com).[26]

Membranes

  • Squamous metaplasia.
  • Chorioamnionitis - see infection section.

Amnion nodosum

General

  • Associated with (long-standing) oligohydramnios.[27]
  • Should be separated from squamous metaplasia of amnion.

Gross

  • Yellow patch or yellow nodules.
    • Some think they are white.[28]

Image: Amnion nodosum (webpathology.com).

Microscopic

Features:

  • Simple epithelium of amnion replaced by (non-keratinizing) stratified squamous epithelium.

Image: Amnion nodosum (webpathology.com).

Passage of meconium

General

  • Associated with fetal distress.
  • Small amount - at term - is considered to be normal.

Gross

  • Green/green discolourization.

Microscopy

Features:[29]

  • Meconium histiocytes - key feature.
    • Macrophages with brown fine granular pigment.
  • Pseudostratified epithelium (amnion) - low power.
  • Amnion - columnar morphology (normally cuboidal).
  • "Drop-out" of individual amnion cells / loss of individual cells.

Time of meconium passage:[30]

  • <1 h - no staining of membranes.
  • 1-3 h - amnion is stained.
  • >3 h - chorion is stained.

DDx:

  • Hemosiderin-laden macrophages.
    • This is sorted-out with an iron stain -- see below.

Notes:

  • The above time course is disputed - in vitro experiments suggest it is considerably longer.[31]


Images:

Special stains

  • Hemosiderin +ve in hemosiderin-laden macrophages.
  • PAS +ve in meconium-laden macrophages.[32]

Useful to differentiate hemosiderin-laden macrophages and meconium laden macrophages:

  • Hemosiderin stain -- +ve for old blood.
    • Prussian-blue stain = hemosiderin stain.[33]

Notes:

  • PAS-D -- +ve in meconium... though may rarely stain hemosiderin.
  • Meconium contains bile.[34]

Squamous metaplasia

  • Benign common finding - no clinical significance.[35]
  • Needs to be separated from amnion nodosum.[36]

Image:

Twin placentas

Main article: Twin placentas

These are often submitted... even if they are normal. In these specimens, usually, the chorion is the key.

It covers:

  • Monozygotic vs. dizygotic twins.
  • Twin-to-twin transfusion syndrome.

Placental disc

Villous edema

General

  • Non-specific finding.

Microscopic

Features:

  • "Swiss chesse-like" appearance / bubbly appearance.
  • Usu. patchy and focal.

DDx:

    • Chorioamnionitis, fetal edema, idiopathic (no cause apparent).

Image:

Diseases of the placental attachment

Placenta creta

  • What?
    • Trophoblastic tissue deeper than it should be.
  • Clinical?
    • Postpartum hemorrhage leading to a hysterectomy.[39]
  • Pathogenesis?
    • It is suspected that it arises as there is defect in the endometrium/myometrium -- not deep trophoblastic invasion.[39]

Note:

  • Normal: trophoblastic tissue attaches to the decidua.[40]

Placenta accreta

  • Trophoblastic tissue (directly) adherent to the myometrium.[40]

Placenta increta

  • Trophoblastic tissue entends into the myometrium.

Placenta increta

  • Trophoblastic tissue penetrates through the myometrium.

Placental abruption

General

Classic clinical manifestations:[41]

  • Vaginal bleeding (~70%).
  • Abdominal pain (~50%).
  • Fetal heart rate abnormalities (~70%).

Sign-out:

  • Pathologists should sign-out this as "focal adherent retroplacental hematoma".
    • The pathologic findings may be due to abruption or manual removal of the placenta.

Gross

Features:[42]

  • Large adherent blood clot.
  • Disc depression on maternal side.

Notes:

  • Loosely attached clot less convincing.
  • Central haemorrhage is the most worrisome.

Microscopic

Features:

  1. Decidual hemorrhage.
    • Blood in the decidua.
  2. Intravillous hemorrhage, AKA villous stromal hemorrhage.
    • "Bags of blood" - blood outside of vessels in the villi.
      • Should not be confused with congested villi.

Notes:

  • There are no definitive microscopic findings for placental abruption.
  • Intravillous hemorrhage is non-specific - may arise in the following: early placental infarct, cord compression, abdominal trauma.

Inflammatory pathologies

Infection

General:[43]

  • Infection usually ascending, i.e. from vagina up through cervix.
    • Associated with intercourse.
  • Hematogenous rare - manifest as villitis.
  • Funisitis usually follows chorioamnionitis.
    • Inflammatory cells in umbilical cord are fetal (trivia).

Types (by site)[43]

  • Fetal membranes: chorioamnionitis, membranitis.[44]
  • Umbilical cord: funisitis.
  • Placenta: placentitis, villitis.

Grading infection (chorioamnionitis, membranitis, funisitis)

Membranitis:[44]

  1. PMNs - decidua only.
  2. PMNs - in subamniotic tissue.
  3. 1 or 2 + necrosis in decidua or chorion/subamniotic tissue.

Chorioamnionitis:[44]

  1. placental chorionic plate only.
  2. 1 + subamniotic tissue.
  3. 1 or 2 + necrosis or abscess.

Sternberg separates vasculitis and funisitis without really explaining the terms[44] -- I presume: vasculitis = inflammation of vessels in the umbilical cord. funisitis = inflammation of the cord (vessels and Wharton jelly).

Umbilical cord vasculitis:[44]

  • +0.5 for each vessel.
  • +0.5 for each vessel with severe involvement.

Umbilical funisitis:[44]

  1. Focal inflammation.
  2. Diffuse inflammation.
  3. Necrosis - in vessels or Wharton jelly.

Note: There is no such thing as chorionitis.[45]

Villitis of unknown etiology

  • Abbreviated VUE.

General

Features:[46]

  • Usually term placenta.
  • Prevalence: 5% to 15% of all placentas.
  • Associated with:

Etiology:

  • Unknown - as the name of the entity suggests.
    • Suspected to be immune-mediated.

Microscopic

Features:[46]

  • Lymphocytes in villous stroma - key feature.
    • Usually focal/patchy.
    • Lymphocytes: maternal derivation, T-lymphocytes -- mostly CD8-positive.
  • +/-Intervillositis (lymphocytes between villi).
  • +/-Histiocytes.

Notes:

  • Lymphocytes are smaller and stain darker than the cells of the villi. (???)
  • Neutrophils are usually absent. A significant number of 'em is suggestive of an infectious villitis.
  • Infective villitis is usu. B-cell predominant.
  • No plasma cells - this suggests an infectious etiology.[48]
    • Plasma cells may be seen in the decidua -- these can be ignored.


Images:

Intervillitis

General

  • Rare.
  • Massive chronic intervillitis - associated IUGR, spontaneous abortion, perinatal fetal death.[51]
  • Recurs.

Microscopic

Features:[51]

  • Intervillous inflammatory cells:
    • Lymphocytes.
    • Histiocytes.
  • Fibrinoid deposition.

Images:

Infarction

True infarcts

General

  • Associated with retroplacental hematoma.

Note: "Maternal floor infarct" is not a true infarct.[52]

Gross

Features:[23]

  • Early - red.
  • Late - white/grey.

Images:

Microscopic

Features:

  1. Necrosis of villi; hyaline material (acellular eosinophilic material) replaces the stroma of the villi.
  2. Loss of intervillous space.[23]
    • Villi appear to be crowded.[53]
      • Normal spacing is ~1x smallest villus or larger.
        • In perivillous fibrin deposition - spacing usu. larger than normal.
  3. Prominent syncytial knots.
  4. Thickened trophoblastic basement membrane (below cytotrophoblasts).
  5. +/-Changes seen in decidual vasculopathy:

Images:

Significant infarcts

  • > 3cm --or-- central location --or-- in 1st or 2nd trimester.
    • Small foci are accepted in term placentae - typically at periphery.

Perivillous fibrin deposition

General

  • Massive perivillous fibrin deposition is assoc. with anti-phospholipid antibody (APLA) syndrome.[55]
    • APLA is assoc. with recurrent miscarriage - can be treated with heparin + ASA.[55]
  • Thought to be an immunologic problem - resulting in platelet activation and fibrin deposition.[55]

Gross

  • Pale (white).
  • Firm.
  • White fibrous sepatae.

Microscopic

Features:

  • Acellular eosinophilic material around formed villi.
  • Obliteration of intervillous space.
    • Intervillous distance increased vis-a-vis normal - key feature.

Notes:

  • Nuclei of villi are usu. preserved.
  • Villi may have secondary infarction, i.e. there may be nuclear destruction (karyolysis, karyorrhexis, pyknosis).

Maternal floor infarct

  • Formally placental maternal floor infarction.

General

  • Not a true infact.
    • It is really fibrin deposition.[52]
  • Associated with intrauterine growth restriction (IUGR).[56]

Microscopic

Features:

Images:

Fetal disease

Fetal thrombotic vasculopathy

General

  • May cause IUGR.
  • Associated with cerebral palsy and common in perinatal deaths.[57]

Microscopic

Features:[57]

  • Thrombus in the fetal vasculature +/- recanalization.
    • Eosinophilic (light pink on H&E), moderately granular intravascular material (fibrin) with layering.
  • Clustered fibrotic villi without blood vessels - key feature.
    • This is a chronic change.

Images:

Hemorrhagic endovasculitis

  • Abbreviated HEV.

General

  • Associated with stillbirth.[60]

Microscopic

Features:[61]

  • Walls of the (fetal) placental blood vessels (in the villi) are disrupted.
  • +/-Intraluminal necrotic debris.
  • RBC fragmentation.

Maternal disease

Hypertensive changes

General

Associated pathologic changes:[62]

  • Placental infarcts.
  • Increased syncytial knots.
  • Hypovascularity of the villi.
  • Cytotrophoblastic proliferation.
  • Thickening of the trophoblastic basement membrane.

Microscopic

Features:[62]

  • Enlarged endothelial cells - fetal capillaries.
  • Atherosis of the spiral arteries - placental bed (maternal).

Notes:

  • One should look for the changes in the membrane roll, not the maternal surface.[63]

Hypertrophic decidual vasculopathy

General

  • A change seen in hypertension.
  • Seen in intrauterine growth restriction (IUGR).

Microscopic

Features:[56]

  • Mild or moderate:
    1. Perivascular inflammatory cells.
    2. +/-Vascular thrombosis.
    3. Smooth muscle hypertrophy.
    4. Endothelial hyperplasia.
      • Above two lead to narrowing of the decidual spiral arteries[64] -- key feature.
  • Severe:[56]
    1. Atherosis of maternal blood vessels.
      • Foamy macrophages within vascular wall.
    2. Fibrinoid necrosis of vessel wall (amorphous eosinophilic material vessel wall).

Note:

  • Smooth muscle hypertrophy can also be understood as lack of physiological conversion of spiral arteries of the uterus.[65]

Images:

HELLP syndrome

General

  • Diagnosed clinically.
  • Pathologically not the same as severe preclampsia.[66]

Definition:

  • H = hemolysis.
  • EL = elevated liver enzymes.
  • LP = low platelets.

Microscopic

Features:[67]

  • Thrombotic microangiopathic vasculopathy.
    • In essence: severe hypertrophic decidual vasculopathy. (???)

Malaria

General

  • Uncommon in Canada.
  • May lead to fetal demise.

Microscopic

Feature:

  • RBCs with basophilic dots ~1-2 micrometres.

Image:

Tumours

Main article: Gestational trophoblastic disease

Chorangioma

General

Epidemiology:

  • Often benign/insignificant; large lesions (>4 cm[68] or >5 cm[69]) or multiple lesions are significant.
  • May be association with:
    • Fetal maternal haemorrhage.
    • Hydrops.
    • IUGR.
  • Incidence: ~1 in 100 placentas.[68]

Gross

  • White lesions.
    • Occasionally red lesions.

Microscopic

Features:[68]

  • Mass of capillaries - key feature.
  • +/-High cellularity.
  • +/-Degenerative changes.

Images:

Notes:

  • Must be differentiated from chorangiomatosis (assoc. with preeclampsia & IUGR) and chorangiosis (assoc. with maternal diabetes mellitus).[68]

Chorangiosis

General

  • Should not be confused with chorangioma.
  • Relative common among babies in ICU ~5%.[70]

Associations:

Microscopic

Features:

  • Increased blood vessels in the terminal villi.
    • Altshuler criteria: "a minimum of 10 villi, each with 10 or more vascular channels, in 10 or more areas of 3 or more random, non-infarcted placental areas when using a ×10 ocular."[72][73]
      • The definition suffers from IPFitis.
  • Lesion not well circumscribed.
  • Villi tend to be larger and have centrally placed blood vessels.[74]

Notes:

  • Usually not seen on gross pathology.
  • Normal villi have up to five vascular channels.[73]

Images:

See also

References

  1. ↑ Yetter JF (March 1998). "Examination of the placenta". Am Fam Physician 57 (5): 1045–54. PMID 9518951.
  2. ↑ Hargitai B, Marton T, Cox PM (August 2004). "Best practice no 178. Examination of the human placenta". J. Clin. Pathol. 57 (8): 785–92. doi:10.1136/jcp.2003.014217. PMC 1770400. PMID 15280396. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770400/.
  3. ↑ URL: http://smj.sma.org.sg/5012/5012ra1.pdf. Accessed on: 11 February 2011.
  4. ↑ CS. 8 February 2011.
  5. ↑ URL: http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=5069. Accessed on: 7 July 2010.
  6. ↑ 6.0 6.1 6.2 6.3 Sternberg, Stephen S. (1997). Histology for Pathologists (2nd ed.). Lippincott Williams & Wilkins. pp. 974. ISBN 978-0397517183.
  7. ↑ Sternberg, Stephen S. (1997). Histology for Pathologists (2nd ed.). Lippincott Williams & Wilkins. pp. 977. ISBN 978-0397517183.
  8. ↑ J Anat. Soc. India 49(2) 149-152 (2000). Available at: http://www.indmedica.com/anatomy/aindex1.cfm?anid=41. Accessed on: January 21, 2009.
  9. ↑ Winters R, Waters BL (December 2008). "What is adequate sampling of extraplacental membranes?: a randomized, prospective analysis". Arch. Pathol. Lab. Med. 132 (12): 1920–3. PMID 19061291.
  10. ↑ Lester, Susan Carole (2005). Manual of Surgical Pathology (2nd ed.). Saunders. pp. 461. ISBN 978-0443066450.
  11. ↑ CS. 7 February 2011.
  12. ↑ AFIP Placental pathol. ISBN: 1-881041-89-1. P.312
  13. ↑ AFIP Placental pathol. ISBN: 1-881041-89-1. P.312
  14. ↑ Fox, Harold; Sebire, Neil J. (2007). Pathology of the Placenta (Major Problems in Pathology) (3rd ed.). Saunders. pp. 559-561. ISBN 978-1416025924.
  15. ↑ 15.0 15.1 15.2 15.3 15.4 15.5 Humphrey, Peter A; Dehner, Louis P; Pfeifer, John D (2008). The Washington Manual of Surgical Pathology (1st ed.). Lippincott Williams & Wilkins. pp. 464. ISBN 978-0781765275.
  16. ↑ Srinivasan R, Arora RS (January 2005). "Do well infants born with an isolated single umbilical artery need investigation?". Arch. Dis. Child. 90 (1): 100–1. doi:10.1136/adc.2004.062372. PMC 1720078. PMID 15613529. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1720078/.
  17. ↑ Lilja M (July 1994). "Infants with single umbilical artery studied in a national registry. 3: A case control study of risk factors". Paediatr Perinat Epidemiol 8 (3): 325–33. PMID 7997408.
  18. ↑ URL: http://www.glowm.com/?p=glowm.cml/section_view&articleid=151. Accessed on: 8 January 2011.
  19. ↑ 19.0 19.1 Hasegawa J, Farina A, Nakamura M, et al. (December 2010). "Analysis of the ultrasonographic findings predictive of vasa previa". Prenat. Diagn. 30 (12-13): 1121–5. doi:10.1002/pd.2618. PMID 20872421.
  20. ↑ 20.0 20.1 Airas U, Heinonen S (April 2002). "Clinical significance of true umbilical knots: a population-based analysis". Am J Perinatol 19 (3): 127–32. doi:10.1055/s-2002-25311. PMID 12012287.
  21. ↑ 21.0 21.1 Humphrey, Peter A; Dehner, Louis P; Pfeifer, John D (2008). The Washington Manual of Surgical Pathology (1st ed.). Lippincott Williams & Wilkins. pp. 464. ISBN 978-0781765275.
  22. ↑ CS. 7 February 2011.
  23. ↑ 23.0 23.1 23.2 23.3 Humphrey, Peter A; Dehner, Louis P; Pfeifer, John D (2008). The Washington Manual of Surgical Pathology (1st ed.). Lippincott Williams & Wilkins. pp. 465. ISBN 978-0781765275.
  24. ↑ Khong TY (December 2010). "Evidence-based pathology: umbilical cord coiling". Pathology 42 (7): 618–22. doi:10.3109/00313025.2010.520309. PMID 21080869.
  25. ↑ PMID 16076615.
  26. ↑ URL: http://flylib.com/books/en/2.953.1.49/1/. Accessed on: 10 January 2011.
  27. ↑ URL: http://library.med.utah.edu/WebPath/PLACHTML/PLAC042.html. Accessed on: 12 January 2011.
  28. ↑ CS. 7 February 2011.
  29. ↑ ALS. 6 Febraury 2009.
  30. ↑ Miller PW, Coen RW, Benirschke K (October 1985). "Dating the time interval from meconium passage to birth". Obstet Gynecol 66 (4): 459–62. PMID 2413412.
  31. ↑ Funai EF, Labowsky AT, Drewes CE, Kliman HJ (January 2009). "Timing of fetal meconium absorption by amnionic macrophages". Am J Perinatol 26 (1): 93–7. doi:10.1055/s-0028-1103028. PMID 19031358.
  32. ↑ Povýsil C, Bennett R, Povýsilová V (January 2001). "CD 68 positivity of the so-called meconium corpuscles in human foetal intestine". Cesk Patol 37 (1): 7–9. PMID 11268705.
  33. ↑ Sienko A, Altshuler G (September 1999). "Meconium-induced umbilical vascular necrosis in abortuses and fetuses: a histopathologic study for cytokines". Obstet Gynecol 94 (3): 415?0. PMID 10472870.
  34. ↑ Sienko A, Altshuler G (September 1999). "Meconium-induced umbilical vascular necrosis in abortuses and fetuses: a histopathologic study for cytokines". Obstet Gynecol 94 (3): 415?0. PMID 10472870.
  35. ↑ Humphrey, Peter A; Dehner, Louis P; Pfeifer, John D (2008). The Washington Manual of Surgical Pathology (1st ed.). Lippincott Williams & Wilkins. pp. 463. ISBN 978-0781765275.
  36. ↑ CS. 7 February 2011.
  37. ↑ URL: http://flylib.com/books/en/2.953.1.49/1/. Accessed on: 10 January 2011.
  38. ↑ URL: http://www.med.yale.edu/obgyn/kliman/placenta/articles/EOR_Placenta/Trophtoplacenta.html. Accessed on: 28 May 2011.
  39. ↑ 39.0 39.1 Tantbirojn, P.; Crum, CP.; Parast, MM. (Jul 2008). "Pathophysiology of placenta creta: the role of decidua and extravillous trophoblast.". Placenta 29 (7): 639-45. doi:10.1016/j.placenta.2008.04.008. PMID 18514815.
  40. ↑ 40.0 40.1 Böcker, Werner; Denk, Helmut; Heitz, Philipp U.; Moch, Holger (2008). [Pathologie] (4th ed.). Urban & Fischer Verlag/Elsevier GmbH. pp. 974. ISBN 978-3437423826.
  41. ↑ Tikkanen M, Nuutila M, Hiilesmaa V, Paavonen J, Ylikorkala O (2006). "Clinical presentation and risk factors of placental abruption". Acta Obstet Gynecol Scand 85 (6): 700–5. doi:10.1080/00016340500449915. PMID 16752262.
  42. ↑ CS. 7 February 2011.
  43. ↑ 43.0 43.1 Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 1106. ISBN 0-7216-0187-1.
  44. ↑ 44.0 44.1 44.2 44.3 44.4 44.5 Mills, Stacey E; Carter, Darryl; Greenson, Joel K; Oberman, Harold A; Reuter, Victor E (2004). Sternberg's Diagnostic Surgical Pathology (4th ed.). Lippincott Williams & Wilkins. pp. 2311. ISBN 978-0781740517.
  45. ↑ ALS. February 2009.
  46. ↑ 46.0 46.1 Redline RW (October 2007). "Villitis of unknown etiology: noninfectious chronic villitis in the placenta". Hum. Pathol. 38 (10): 1439–46. doi:10.1016/j.humpath.2007.05.025. PMID 17889674.
  47. ↑ Feeley L, Mooney EE (2010). "Villitis of unknown aetiology: correlation of recurrence with clinical outcome". J Obstet Gynaecol 30 (5): 476–9. doi:10.3109/01443611003802339. PMID 20604650.
  48. ↑ CS. 7 February 2011.
  49. ↑ URL: http://jcp.bmj.com/content/61/12/1254.abstract. Accessed on: 11 January 2011.
  50. ↑ 50.0 50.1 URL: http://www.flickr.com/photos/jian-hua_qiao_md/3954021698/. Accessed on: 11 January 2011.
  51. ↑ 51.0 51.1 Rota, C.; Carles, D.; Schaeffer, V.; Guyon, F.; Saura, R.; Horovitz, J. (Nov 2006). "[Perinatal prognosis of pregnancies complicated by placental chronic intervillitis].". J Gynecol Obstet Biol Reprod (Paris) 35 (7): 711-9. PMID 17088773.
  52. ↑ 52.0 52.1 Weedman Molavi, Diana (2008). The Practice of Surgical Pathology: A Beginner's Guide to the Diagnostic Process (1st ed.). Springer. pp. 178. ISBN 978-0387744858.
  53. ↑ Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.; Abbas, Abul K. (2005). Robbins and Cotran pathologic basis of disease (7th ed.). St. Louis, Mo: Elsevier Saunders. pp. 1109. ISBN 0-7216-0187-1.
  54. ↑ URL: http://path.upmc.edu/cases/case75/micro.html. Accessed on: 6 January 2011.
  55. ↑ 55.0 55.1 55.2 Sebire NJ, Backos M, Goldin RD, Regan L (May 2002). "Placental massive perivillous fibrin deposition associated with antiphospholipid antibody syndrome". BJOG 109 (5): 570–3. PMID 12066949. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=1470-0328&date=2002&volume=109&issue=5&spage=570.
  56. ↑ 56.0 56.1 56.2 Roberts, DJ.; Post, MD. (Dec 2008). "The placenta in pre-eclampsia and intrauterine growth restriction.". J Clin Pathol 61 (12): 1254-60. doi:10.1136/jcp.2008.055236. PMID 18641412.
  57. ↑ 57.0 57.1 Kraus FT, Acheen VI (July 1999). "Fetal thrombotic vasculopathy in the placenta: cerebral thrombi and infarcts, coagulopathies, and cerebral palsy". Hum. Pathol. 30 (7): 759–69. PMID 10414494. Cite error: Invalid <ref> tag; name "pmid10414494" defined multiple times with different content
  58. ↑ URL: http://jcp.bmj.com/content/61/12/1254.abstract. Accessed on: 12 January 2011.
  59. ↑ URL: http://gut.bmj.com/content/41/3/354.full. Accessed on: 12 January 2011.
  60. ↑ Stevens NG, Sander CH (October 1984). "Placental hemorrhagic endovasculitis: risk factors and impact on pregnancy outcome". Int J Gynaecol Obstet 22 (5): 393–7. PMID 6151926.
  61. ↑ Sander CM, Gilliland D, Akers C, McGrath A, Bismar TA, Swart-Hills LA (February 2002). "Livebirths with placental hemorrhagic endovasculitis: interlesional relationships and perinatal outcomes". Arch. Pathol. Lab. Med. 126 (2): 157–64. PMID 11825110.
  62. ↑ 62.0 62.1 Soma H, Yoshida K, Mukaida T, Tabuchi Y (1982). "Morphologic changes in the hypertensive placenta". Contrib Gynecol Obstet 9: 58–75. PMID 6754249.
  63. ↑ CS. 7 February 2011.
  64. ↑ AFIP - Placental Pathology. P.122. ISBN: 1-881041-89-1. 2004.
  65. ↑ Naicker, T.; Khedun, SM.; Moodley, J.; Pijnenborg, R. (Aug 2003). "Quantitative analysis of trophoblast invasion in preeclampsia.". Acta Obstet Gynecol Scand 82 (8): 722-9. PMID 12848643.
  66. ↑ Vinnars MT, Wijnaendts LC, Westgren M, Bolte AC, Papadogiannakis N, Nasiell J (May 2008). "Severe preeclampsia with and without HELLP differ with regard to placental pathology". Hypertension 51 (5): 1295–9. doi:10.1161/HYPERTENSIONAHA.107.104844. PMID 18362224.
  67. ↑ Ornstein MH, Rand JH (July 1994). "An association between refractory HELLP syndrome and antiphospholipid antibodies during pregnancy; a report of 2 cases". J. Rheumatol. 21 (7): 1360–4. PMID 7966086.
  68. ↑ 68.0 68.1 68.2 68.3 68.4 Amer HZ, Heller DS (2010). "Chorangioma and related vascular lesions of the placenta--a review". Fetal Pediatr Pathol 29 (4): 199–206. doi:10.3109/15513815.2010.487009. PMID 20594143.
  69. ↑ Lež C, Fures R, Hrgovic Z, Belina S, Fajdic J, Münstedt K (2010). "Chorangioma placentae". Rare Tumors 2 (4): e67. doi:10.4081/rt.2010.e67. PMC 3019602. PMID 21234259. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3019602/.
  70. ↑ URL: http://www.bhj.org/journal/2009_5102_april/download/pg251-252.pdf. Accessed on: 26 July 2011.
  71. ↑ Daskalakis, G.; Marinopoulos, S.; Krielesi, V.; Papapanagiotou, A.; Papantoniou, N.; Mesogitis, S.; Antsaklis, A. (2008). "Placental pathology in women with gestational diabetes.". Acta Obstet Gynecol Scand 87 (4): 403-7. doi:10.1080/00016340801908783. PMID 18382864.
  72. ↑ Altshuler, G. (Jan 1984). "Chorangiosis. An important placental sign of neonatal morbidity and mortality.". Arch Pathol Lab Med 108 (1): 71-4. PMID 6546343.
  73. ↑ 73.0 73.1 De La Ossa, MM.; Cabello-Inchausti, B.; Robinson, MJ. (Sep 2001). "Placental chorangiosis.". Arch Pathol Lab Med 125 (9): 1258. doi:10.1043/0003-9985(2001)1251258:PC2.0.CO;2. PMID 11520290. http://www.archivesofpathology.org/doi/full/10.1043/0003-9985%282001%29125%3C1258:PC%3E2.0.CO;2.
  74. ↑ E. Latta. 26 July 2011.

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