Placenta
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).
- Location: central, eccentric, marginal.
- 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.
- Attachment.
- 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]
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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.
- Pathologic findings (gross): depression on maternal side, large blood clot.
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:[12]
- PMNs - decidua only.
- PMNs - in subamniotic tissue.
- 1 or 2 + necrosis in decidua or chorion/subamniotic tissue.
Chorioamnionitis:[12]
- placental chorionic plate only.
- 1 + subamniotic tissue.
- 1 or 2 + necrosis or abscess.
Sternberg separates vasculitis and funisitis without really explaining the terms[12] -- I presume: vasculitis = inflammation of vessels in the umbilical cord. funisitis = inflammation of the cord (vessels and Wharton jelly).
Umbilical cord vasculitis:[12]
- +0.5 for each vessel.
- +0.5 for each vessel with severe involvement.
Umbilical funisitis:[12]
- focal inflammation.
- diffuse inflammation.
- necrosis - in vessels or Wharton jelly.
Note: There is no such thing as chorionitis.[13]
IHC
Useful to differentiate hemosiderin-laden macrophages and meconium laden macrophages:
- Hemosiderin stain -- +ve for old blood.
- Prussian-blue stain = hemosiderin stain.[14]
- PAS-D -- +ve in chorioamnionitis???
Note:
- Meconium contains bile.[15]
Infarction
General
- Associated with retroplacental hematoma.
Gross
Features:[16]
- Early - red.
- Late - white/grey.
Microscopy
Features:
- Loss of intervillous space.[16]
- Villi appear to be crowded.
- 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.[18]
- APLA is assoc. with recurrent miscarriage - can be treated with heparin + ASA.[18]
- Thought to be an immunologic problem - resulting in platelet activation and fibrin deposition.[18]
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[19]
- 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:[20]
- <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.[21]
Placental mass
Placental mass by gestational age:[22]
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[23] 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:[24]
- Enlarged endothelial cells - fetal capillaries.
- Atherosis of the spiral arteries - placental bed (maternal).
Associated changes:[24]
- Placental infarcts.
- Increased syncytial knots.
- Hypovascularity of the villi.
- Cytotrophoblastic proliferation.
- Thickening of the trophoblastic basement membrane.
Hypertrophic decidual vasculopathy
Features:[25]
- Mild or moderate:
- Perivascular inflammatory cells.
- +/-Vascular thrombosis.
- Smooth muscle hypertrophy.
- Endothelial hyperplasia.
- Above two lead to narrowing of the decidual spiral arteries[26] -- key feature.
- Severe:[25]
- Atherosis of maternal blood vessels.
- Foamy macrophages within vascular wall.
- Fibrinoid necrosis of vessel wall (amorphous eosinophilic material vessel wall).
- Atherosis of maternal blood vessels.
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:[27]
- Thrombotic microangiopathic vasculopathy.
- In essence: severe hypertrophic decidual vasculopathy. (???)
Tumours
Clinical screening tests
- PAPP-A - low values seen in aneuploidy.[28]
See also
References
- ↑ Sternberg. Histo. for Pathol. 2nd Ed. P.974
- ↑ H4P 2nd Ed., P.974.
- ↑ H4P 2nd Ed., P.974.
- ↑ H4P 2nd Ed., P.977.
- ↑ H4P 2nd Ed., P.974.
- ↑ 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.
- ↑ Lester 2nd Ed. P.461
- ↑ [1]
- ↑ http://library.med.utah.edu/WebPath/PLACHTML/PLAC042.html
- ↑ Histo. for Pathol. 2nd Ed. P.979
- ↑ 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.
- ↑ 12.0 12.1 12.2 12.3 12.4 12.5 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.
- ↑ ALS Feb 2009
- ↑ 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.
- ↑ 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.
- ↑ 16.0 16.1 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.
- ↑ 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.
- ↑ 18.0 18.1 18.2 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.
- ↑ ALS. 6 Feb 2009.
- ↑ 3 Apr 2009.
- ↑ PMID 11268705
- ↑ AFIP Placental pathol. ISBN: 1-881041-89-1. P.312
- ↑ AFIP Placental pathol. ISBN: 1-881041-89-1. P.312
- ↑ 24.0 24.1 Soma H, Yoshida K, Mukaida T, Tabuchi Y (1982). "Morphologic changes in the hypertensive placenta". Contrib Gynecol Obstet 9: 58–75. PMID 6754249.
- ↑ 25.0 25.1 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.
- ↑ AFIP - Placental Pathology. P.122. ISBN: 1-881041-89-1. 2004.
- ↑ 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.
- ↑ URL: http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=5069. Accessed on: 7 July 2010.