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).

Images:

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

Clinical screening tests

  • PAPP-A - low values seen in aneuploidy.[33]

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.