Placenta

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

Normal

Amnion - next to fetus, surrounds amniotic fluid, avascular.

  • Characterized by a single layer of cells.[1]
    • Cuboidal/squamoid shape.
    • Eosinophilic cytoplasm.
    • Central nucleus.
  • Squamous metaplasia may be seen at cord insertion.
  • Basement membrane.
  • 'Compact layer'.[2]
  • 'Fibroblastic layer'.[3]

Chorion - surrounds amnion

  • Layers:[4]
    • 'Reticular layer' - cellular (inner aspect).
    • 'Pseudo-basemement membrane'.
    • 'Outer trophoblastic layer'.
  • Has blood vessels.
  • Opposed to "trophoblastic X cells" on side opposite of amnion.[5]
    • Beneath of the "trophoblastic X cells" is decidua (mnemonic NEW = nucleus central, eosinophilic, well-defined cell border), which is maternal tissue.

Additional terms

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

Grossing

  • Dimensions:
    • Disc.
    • Length of cord, diameter of cord.
  • Mass (weight) -- should be done 'trimmed' (cord cut-off, membrane cut-off).
  • 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.
    • Number of vessels.
      • Normal: 2 arteries, 1 vein.
  • Membranes - shiny, thin, translucent
    • Attachment: marginal (normal), circummarginate (inside edge), circumvallated (folding on self).
  • Placental disc.
    • Fetal surface - normal is shinny (dull in chorioamnionitis).
    • Maternal surface - are the cotyledons intact?

Sections

  • Cord two sections.
  • Cord at insertion.
  • Membranes (rolled).
  • Placenta - full thickness (maternal and fetal surface).

Placental membranes

Appearance:[7]

  • Normal - shiny.
  • Choriomnionitis - opaque/dull.
  • Meconium - green.
  • Amnion nodosum.
    • AKA squamous metaplasia of amnion.[8]
    • Assoc. with oligohydramnios.[9]
    • Gross: - (single) yellow patch or yellow nodules .

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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).

Twin placentas

No membrane between fetuses.

  • Split at approx. 7th day.

Diamnionic-monochorionic (DiMo)

  • No interposed chorion.[10]
  • Always monozygotic.
  • Highest risk of TTTS (twin-to-twin transfusion syndrome).

Diamnionic-dichorionic (DiDi)

  • Most dizygotic (70%), may be monozygotic (30%).
  • If monozygotic -- split before 3 days.

Bleeding in late pregnancy

DDx of bleeding in late pregnancy:

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

Placental abruption

  • Central haemorrhage is the most worrisome.
    • Pathologic findings (gross): depression on maternal side, large blood clot.
      • There are *no* good microscopic findings.

Infection

Types (by site):[11]

  • Fetal membranes: chorioamnionitis, membranitis.[12]
  • Umbilical cord: funisitis.
  • Placenta: placentitis, villitis.

General:[11]

  • Infection usually ascending, i.e. from vagina up through cervix.
    • Assoc. 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).

Grading infection

Membranitis[13]

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

Chorioamnionitis[14]

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

Umbilical cord vasculitis:[16]

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

Umbilical funisitis:[17]

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

Note: There is no such thing as chorionitis.[18]

IHC

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

  • Hemosiderin stain -- +ve for old blood.
    • Prussian-blue stain = hemosiderin stain.[19]
  • PAS-D -- +ve in chorioamnionitis???

Note:

  • Meconium contains bile.[20]

Infarction

General

  • Associated with retroplacental hematoma.

Gross

Features:[21]

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

Microscopy

Features:

  • Loss of intervillous space.[21]
    • Villi appear to be crowded.

[22]

  • Prominent syncytial knots.
  • Thickened trophoblastic basement membrance (below cytotrophoblasts).
  • +/-Acute atherosis (vaguely like atherosclerosis).
    • Fibrioid necrosis.
    • Vessel wall lipid deposition.

Significant infarcts

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

Chorangioma

General

  • Hemangioma ???

Epidemiology

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

Microscopy

  • Mass of capillaries.


Perivillous fibrin deposition

  • Massive perivillous fibrin deposition is assoc. with anti-phospholipid antibody (APLA) syndrome.[23]
    • APLA is assoc. with recurrent miscarriage - can be treated with heparin + ASA.[23]
  • Thought to be an immunologic problem - resulting in platelet activation and fibrin deposition.[23]

Gross

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

Microscopy

  • Acellular eosinophilic material around formed villi.
    • Obliteration of intervillous space.


Passage of meconium

General

  • Associated with fetal distress.

Gross

  • Green/green discolourization.

Microscopy[24]

  • Macrophages with brown fine granular pigment.
  • Columnar morphology (normally cuboidal).
  • "Drop-out" of individual cell -- the loss of individual cells.

Level of staining and time:[25]

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

Images:

DDx

  • Hemosiderin-laden macrophages.

Special stains

  • Hemosiderin +ve in hemosiderin-laden macrophages.
  • PAS +ve in meconium-laden macrophages.[26]

Placental mass

Placental mass by gestational age:[27]

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[28] 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).

Hypertensive changes

Features:[29]

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

Associated changes:[29]

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

Hypertrophic decidual vasculopathy

Features:[30]

  • 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[31] -- key feature.
  • Severe:[30]
    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).

HELLP syndrome

General

  • Diagnosed clinically.

Definition:

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

Microscopic

Features:[32]

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

Tumours

Main article: Gestational trophoblastic disease

Clinical screening tests

  • PAPP-A - low values seen in aneuploidy.[33]
Main article: Pregnancy

See also

References

  1. ↑ Sternberg. Histo. for Pathol. 2nd Ed. P.974
  2. ↑ H4P 2nd Ed., P.974.
  3. ↑ H4P 2nd Ed., P.974.
  4. ↑ H4P 2nd Ed., P.977.
  5. ↑ H4P 2nd Ed., P.974.
  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 2nd Ed. P.461
  8. ↑ [1]
  9. ↑ http://library.med.utah.edu/WebPath/PLACHTML/PLAC042.html
  10. ↑ Histo. for Pathol. 2nd Ed. P.979
  11. ↑ 11.0 11.1 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.
  12. ↑ Sternberg P.2311
  13. ↑ Sternberg P.2311
  14. ↑ Sternberg P.2311
  15. ↑ Sternberg P.2311.
  16. ↑ Sternberg P.2311
  17. ↑ Sternberg P.2311
  18. ↑ ALS Feb 2009
  19. ↑ 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.
  20. ↑ 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.
  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. 465. ISBN 978-0781765275.
  22. ↑ 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.
  23. ↑ 23.0 23.1 23.2 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.
  24. ↑ ALS. 6 Feb 2009.
  25. ↑ 3 Apr 2009.
  26. ↑ PMID 11268705
  27. ↑ AFIP Placental pathol. ISBN: 1-881041-89-1. P.312
  28. ↑ AFIP Placental pathol. ISBN: 1-881041-89-1. P.312
  29. ↑ 29.0 29.1 Soma H, Yoshida K, Mukaida T, Tabuchi Y (1982). "Morphologic changes in the hypertensive placenta". Contrib Gynecol Obstet 9: 58–75. PMID 6754249.
  30. ↑ 30.0 30.1 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.
  31. ↑ AFIP - Placental Pathology. P.122. ISBN: 1-881041-89-1. 2004.
  32. ↑ 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.
  33. ↑ URL: http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=5069. Accessed on: 7 July 2010.
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