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.

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]

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.[3]
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

Amnion

General:

  • Next to fetus, surrounds amniotic fluid, avascular.

Characteristics:

  • Characterized by a single layer of cells.[4]
    • Cuboidal/squamoid shape.
    • Eosinophilic cytoplasm.
    • Central nucleus.
  • Squamous metaplasia may be seen at cord insertion.
  • Basement membrane.
  • 'Compact layer'.[4]
  • 'Fibroblastic layer'.[4]

Chorion

General:

  • Surrounds amnion.

Characteristics:

  • Layers:[5]
    • 'Reticular layer' - cellular (inner aspect).
    • 'Pseudo-basemement membrane'.
    • 'Outer trophoblastic layer'.
  • Has blood vessels.
  • Opposed to "trophoblastic X cells" on side opposite of amnion.[4]
    • 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[6]
      • 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).
  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:[7]

  • Normal - shiny.
  • Choriomnionitis - opaque/dull.
  • Meconium - green.
  • Amnion nodosum - yellow patches.
    • Some describe 'em as white.[8]

Placental mass

Placental mass by gestational age:[9]

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[10] 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).

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.[11]
    • 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.[12]
  • Associated with maternal diabetes.[13]

Image:

Insertion

Marginal insertion

Definition:

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

Prevalence:

  • Approximately 12% of placentas.[11]

Relevance:

  • None according to WMSP.[11]
    • 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.[15]

Velamentous insertion

Definition:

  • The umbilical cord inserts into the fetal membranes.[11]
    • The vessels are not protected by Wharton's jelly.
      • Wharton's jelly = the connective tissue surrounding the vessels in the cord.

Details:[11]

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

Relevance:

  • Increased risk of vasa previa.[15]

Knots

General

  • Prevalence ~1.25%.[16][17]
  • Increase risk of stillbirth; odds ratio 3.93.[16]

Gross

Work-up:[17]

  • 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.[11]
    • Normal: 1-3 coils/10 cm.[18]
  • Associated with cord stricture, which is usu. at the fetal end of the cord.[19]

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.[20]
    • What are the 10% and 90% cut-points? They are not given in WMSP. UT access to a journal article[21] that might have it is screwed-up.

Cord hematoma

Features:[19]

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

Image: Hematoma (flylib.com).[22]

Membranes

  • Squamous metaplasia.
  • Chorioamnionitis - see infection section.

Amnion nodosum

General

  • Associated with (long-standing) oligohydramnios.[23]
  • Should be separated from squamous metaplasia of amnion.

Gross

  • Yellow patch or yellow nodules.
    • Some think they are white.[24]

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:[25]

  • 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:[26]

  • <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.[27]


Images:

Special stains

  • Hemosiderin +ve in hemosiderin-laden macrophages.
  • PAS +ve in meconium-laden macrophages.[28]

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

  • Hemosiderin stain -- +ve for old blood.
    • Prussian-blue stain = hemosiderin stain.[29]

Notes:

  • PAS-D -- +ve in meconium... though may rarely stain hemosiderin.
  • Meconium contains bile.[30]

Squamous metaplasia

  • Benign common finding - no clinical significance.[31]
  • Needs to be separated from amnion nodosum.[32]

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.

Diseases of the placental attachment

Placenta acreta/percreta/increta

Placenta attaches to the uterus deeper than it should.

Placental abruption

General

Classic clinical manifestations:[34]

  • 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:[35]

  • 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 placenta

Infection

General:[36]

  • Infection usually ascending, i.e. from vagina up through cervix.
    • Associated with intercourse.
  • Hematogenous rare - manifest as villitis.
    • Think TORCH infections (toxoplasmosis, others (syphilis, TB, listeriosis), rubella, cytomegalovirus, herpes simplex virus).
  • Funisitis usually follows chorioamnionitis.
    • Inflammatory cells in umbilical cord are fetal (trivia).

Types (by site)[36]

  • Fetal membranes: chorioamnionitis, membranitis.[37]
  • Umbilical cord: funisitis.
  • Placenta: placentitis, villitis.

Grading infection (chorioamnionitis, membranitis, funisitis)

Membranitis:[37]

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

Chorioamnionitis:[37]

  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[37] -- I presume: vasculitis = inflammation of vessels in the umbilical cord. funisitis = inflammation of the cord (vessels and Wharton jelly).

Umbilical cord vasculitis:[37]

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

Umbilical funisitis:[37]

  1. focal inflammation.
  2. diffuse inflammation.
  3. necrosis - in vessels or Wharton jelly.

Note: There is no such thing as chorionitis.[38]

Villitis of unknown etiology

  • Abbreviated VUE.

General

Features:[39]

  • Usually term placenta.
  • Prevalence: 5% to 15% of all placentas.
  • Associated with:
    • Intrauterine growth restriction.
    • Recurrent reproductive loss -- key point.

Etiology:

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

Microscopic

Features:[39]

  • Lymphocytes in villous stroma - key feature.
    • Usually focal/patchy.
    • Lymphocytes: maternal derivation, T-lymphocytes -- mostly CD8-positive.
  • +/-Intervillositis (lymphocytes between villi).
  • +/-Histiocytes.
  • No plasma cells - this suggests an infectious etiology.[40]
    • Plasma cells may be in the decidua.

Notes:

  • Neutrophils are usually absent. A significant number of 'em is suggestive of an infectious villitis.
  • Infective villitis is usu. B-cell predominant.

Images:

Infarction

True infarcts

General

  • Associated with retroplacental hematoma.

Gross

Features:[19]

  • 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.[19]
    • Villi appear to be crowded.[43]
      • 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 membrance (below cytotrophoblasts).
  5. +/-Changes seen in decidual vasculopathy:
    • Acute atherosis (vaguely like atherosclerosis).
      • Fibrioid necrosis.
      • Vessel wall lipid deposition.

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

  • Massive perivillous fibrin deposition is assoc. with anti-phospholipid antibody (APLA) syndrome.[45]
    • APLA is assoc. with recurrent miscarriage - can be treated with heparin + ASA.[45]
  • Thought to be an immunologic problem - resulting in platelet activation and fibrin deposition.[45]

Gross

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

Microscopy

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).

Fetal disease

Fetal thrombotic vasculopathy

General

  • May cause IUGR.
  • Associated with cerebral palsy and common in perinatal deaths.[46]

Microscopic

Features:

  • Thrombus in the fetal vasculature +/- recanalization.
    • Eosinophilic (light pink on H&E), moderately granular intravascular material (fibrin) with layering.

Images:

Hemorrhagic endovasculitis

  • Abbreviated HEV.

General

  • Associated with stillbirth.[49]

Microscopic

Features:[50]

  • 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:[51]

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

Microscopic

Features:[51]

  • 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.[52]

Hypertrophic decidual vasculopathy

General

  • A change seen in hypertension.

Microscopic

Features:[53]

  • 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[54] -- key feature.
  • Severe:[53]
    1. Atherosis of maternal blood vessels.
      • Foamy macrophages within vascular wall.
    2. Fibrinoid necrosis of vessel wall (amorphous eosinophilic material vessel wall).

General:

  • Seen in intrauterine growth restriction (IUGR).

Images:

HELLP syndrome

General

  • Diagnosed clinically.
  • Pathologically not the same as severe preclampsia.[55]

Definition:

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

Microscopic

Features:[56]

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

Tumours

Main article: Gestational trophoblastic disease

Chorangioma

General

Epidemiology:

  • Often benign.
  • May be association with:
    • Fetal maternal haemorrhage.
    • Hydrops.
    • IUGR.

Gross

  • White lesions.
    • Occasionally red lesions.

Microscopic

Features:

  • Mass of capillaries.

Image:

Chorangiosis=

General

  • Should not be confused with chorangioma.
  • Rare.

Associations:

  • Maternal hypoxia:
    • Smoking.
    • Altitude.
    • Diabetes.

Microscopic

Features:

  • Increased blood vessels in the terminal villi.
  • Not well circumscribed.

Notes:

  • Usually not seen on gross pathology.

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://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=5069. Accessed on: 7 July 2010.
  4. ↑ 4.0 4.1 4.2 4.3 Sternberg, Stephen S. (1997). Histology for Pathologists (2nd ed.). Lippincott Williams & Wilkins. pp. 974. ISBN 978-0397517183.
  5. ↑ Sternberg, Stephen S. (1997). Histology for Pathologists (2nd ed.). Lippincott Williams & Wilkins. pp. 977. ISBN 978-0397517183.
  6. ↑ 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.
  7. ↑ Lester, Susan Carole (2005). Manual of Surgical Pathology (2nd ed.). Saunders. pp. 461. ISBN 978-0443066450.
  8. ↑ CS. 7 February 2011.
  9. ↑ AFIP Placental pathol. ISBN: 1-881041-89-1. P.312
  10. ↑ AFIP Placental pathol. ISBN: 1-881041-89-1. P.312
  11. ↑ 11.0 11.1 11.2 11.3 11.4 11.5 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.
  12. ↑ 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/.
  13. ↑ 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.
  14. ↑ URL: http://www.glowm.com/?p=glowm.cml/section_view&articleid=151. Accessed on: 8 January 2011.
  15. ↑ 15.0 15.1 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.
  16. ↑ 16.0 16.1 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.
  17. ↑ 17.0 17.1 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.
  18. ↑ CS. 7 February 2011.
  19. ↑ 19.0 19.1 19.2 19.3 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.
  20. ↑ Khong TY (December 2010). "Evidence-based pathology: umbilical cord coiling". Pathology 42 (7): 618–22. doi:10.3109/00313025.2010.520309. PMID 21080869.
  21. ↑ PMID 16076615.
  22. ↑ URL: http://flylib.com/books/en/2.953.1.49/1/. Accessed on: 10 January 2011.
  23. ↑ URL: http://library.med.utah.edu/WebPath/PLACHTML/PLAC042.html. Accessed on: 12 January 2011.
  24. ↑ CS. 7 February 2011.
  25. ↑ ALS. 6 Febraury 2009.
  26. ↑ 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.
  27. ↑ 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.
  28. ↑ 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.
  29. ↑ 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.
  30. ↑ 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.
  31. ↑ 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.
  32. ↑ CS. 7 February 2011.
  33. ↑ URL: http://flylib.com/books/en/2.953.1.49/1/. Accessed on: 10 January 2011.
  34. ↑ 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.
  35. ↑ CS. 7 February 2011.
  36. ↑ 36.0 36.1 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.
  37. ↑ 37.0 37.1 37.2 37.3 37.4 37.5 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.
  38. ↑ ALS. February 2009.
  39. ↑ 39.0 39.1 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.
  40. ↑ CS. 7 February 2011.
  41. ↑ URL: http://jcp.bmj.com/content/61/12/1254.abstract. Accessed on: 11 January 2011.
  42. ↑ URL: http://www.flickr.com/photos/jian-hua_qiao_md/3954021698/. Accessed on: 11 January 2011.
  43. ↑ 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.
  44. ↑ URL: http://path.upmc.edu/cases/case75/micro.html. Accessed on: 6 January 2011.
  45. ↑ 45.0 45.1 45.2 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.
  46. ↑ 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.
  47. ↑ URL: http://jcp.bmj.com/content/61/12/1254.abstract. Accessed on: 12 January 2011.
  48. ↑ URL: http://gut.bmj.com/content/41/3/354.full. Accessed on: 12 January 2011.
  49. ↑ 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.
  50. ↑ 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.
  51. ↑ 51.0 51.1 Soma H, Yoshida K, Mukaida T, Tabuchi Y (1982). "Morphologic changes in the hypertensive placenta". Contrib Gynecol Obstet 9: 58–75. PMID 6754249.
  52. ↑ CS. 7 February 2011.
  53. ↑ 53.0 53.1 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.
  54. ↑ AFIP - Placental Pathology. P.122. ISBN: 1-881041-89-1. 2004.
  55. ↑ 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.
  56. ↑ 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.
  57. ↑ 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.

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